Stem cell stories that caught our eye: glowing stem cells and new insights into Zika and SCID

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Glowing stem cells help scientists understand how cells work. (Karen Ring)
It’s easy to notice when something is going wrong. It’s a lot harder to notice when something is going right. The same thing can be said for biology. Scientists dedicate their careers to studying unhealthy cells, trying to understand why people get certain diseases and what’s going wrong at the cellular level to cause these problems. But there is a lot to be said for doing scientific research on healthy cells so that we can better understand what’s happening when cells start to malfunction.

A group from the Allen Institute for Cell Science is doing just this. They used a popular gene-editing technology called CRISPR/Cas9 to genetically modify human stem cell lines so that certain parts inside the cell will glow different colors when observed under a fluorescent microscope. Specifically, the scientists inserted the genetic code to produce fluorescent proteins in both the nucleus and the mitochondria of the stem cells. The final result is a tool that allows scientists to study how stem cells specialize into mature cells in various tissues and organs.

Glowing human stem cells. The edges of the cells are shown in purple while the DNA in the cell’s nucleus is in blue. (Allen Institute for Cell Science).

Glowing human stem cells. The edges of the cells are shown in purple while the DNA in the cell’s nucleus is in blue. (Allen Institute for Cell Science).

The director of stem cells and gene editing at the Allen Institute, Ruwanthi Gunawardane, explained how their technology improves upon previous methods for getting cells to glow in an interview with Forbes:

 “We’re trying to understand how the cell behaves, how it functions, but flooding it with some external protein can really mess it up. The CRISPR system allows us to go into the DNA—the blueprint—and insert a gene that allows the cell to express the protein in its normal environment. Then, through live imaging, we can watch the cell and understand how it works.”

The team has made five of these glowing stem cell lines available for use by the scientific community through the Coriell Institute for Medical Research (which also works closely with the CIRM iPSC Initiative). Each cell line is unique and has a different cellular structure that glows. You can learn more about these cell lines on the Coriell Allen Institute webpage and by watching this video:

 

Zika can take multiple routes to infect a child’s brain. (Kevin McCormack)
One of the biggest health stories of 2016 has been the rapid, indeed alarming, spread of the Zika virus. It went from an obscure virus to a global epidemic found in more than 70 countries.

The major concern about the virus is its ability to cause brain defects in the developing brain. Now researchers at Harvard have found that it can do this in more ways than previously believed.

Up till now, it was believed that Zika does its damage by grabbing onto a protein called AXL on the surface of brain cells called neural progenitor cells (NPCs). However, the study, published in the journal Cell Stem Cell, showed that even when AXL was blocked, Zika still managed to infiltrate the brain.

Using induced pluripotent stem cell technology, the researchers were able to create NPCs and then modify them so they had no AXL expression. That should, in theory, have been able to block the Zika virus. But when they exposed those cells to the virus they found they were infected just as much as ordinary brain cells exposed to the virus were.

Caption: Zika virus (light blue) spreads through a three-dimensional model of a developing brain. Image by Max Salick and Nathaniel Kirkpatrick/Novartis

Caption: Zika virus (light blue) spreads through a three-dimensional model of a developing brain. Image by Max Salick and Nathaniel Kirkpatrick/Novartis

In a story in the Harvard Gazette, Kevin Eggan, one of the lead researchers, said this shows scientists need to re-think their approach to countering the virus:

“Our finding really recalibrates this field of research because it tells us we still have to go and find out how Zika is getting into these cells.”

 

Treatment for a severe form of bubble baby disease appears on the horizon. (Todd Dubnicoff)
Without treatment, kids born with bubble baby disease typically die before reaching 12 months of age. Formally called severe combined immunodeficiency (SCID), this genetic blood disorder leaves infants without an effective immune system and unable to fight off even minor infections. A bone marrow stem cell transplant from a matched sibling can treat the disease but this is only available in less than 20 percent of cases and other types of donors carry severe risks.

In what is shaping up to be a life-changing medical breakthrough, a UCLA team has developed a stem cell/gene therapy treatment that corrects the SCID mutation. Over 40 patients have participated to date with a 100% survival rate and CIRM has just awarded the team $20 million to continue clinical trials.

There’s a catch though: other forms of SCID exist. The therapy described above treats SCID patients with a mutation in a gene responsible for producing a protein called ADA. But an inherited mutation in another gene called Artemis, leads to a more severe form of SCID. These Artemis-SCID infants have even less success with a standard bone marrow transplant compared to those with ADA-SCID. Artemis plays a role in DNA damage repair something that occurs during the chemo and radiation therapy sessions that are often necessary for blood marrow transplants. So Artemis-SCID patients are hyper-sensitive to the side of effects of standard treatments.

A recent study by UCSF scientists in Human Gene Therapy, funded in part by CIRM, brings a lot of hope to these Artemis-SCID patient. Using a similar stem cell/gene therapy method, this team collected blood stem cells from the bone marrow of mice with a form of Artemis-SCID. Then they added a good copy of the human Artemis gene to these cells. Transplanting the blood stem cells back to mice, restored their immune systems which paves the way for delivering this approach to clinic to also help the Artemis-SCID patients in desperate need of a treatment.

Stem cell stories that caught our eye: Horse patients, Brain cancer stem cells, and a Bony Heart

Horsing around at the World Stem Cell Summit
The World Stem Cell Summit (WSCS) is coming up very shortly (December 6-9) in lovely downtown West Palm Beach, Florida. And this year it has an added attraction; horses.

For my money the WSCS is the most enjoyable of the many conferences held around the US focusing on stem cells. Most conferences have either scientists or patients and patient advocates. This brings them both together creating an event that highlights the science, the people doing it, and the people who hope to benefit from it.

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Eadweard Muybridge’s Galloping Horse
Image: Wikimedia Commons

And this year it’s not just about people, it’s also about horses. For the first time the event will feature the Equine World Stem Cell Summit. This makes sense on so many levels. Animals, large and small, have always been an important element in advancing scientific research, enabling us to test treatments and make sure they are safe before trying them out on people.

But horses are also athletes and sports has always been a powerful force in accelerating research. When you think about the “Sport of Kings” and how much money is involved in breeding and racing horses it’s not surprising that rich owners are always looking for new treatments that can help their thoroughbreds recover from injuries.

And if they help repair damaged bones and tendons in thoroughbreds, who’s to say those techniques and that research couldn’t help the rest of us.

Loss of gene allows cancer stem cells to invade the brain
A fundamental property of stem cells is their ability to self-renew and make unlimited copies of themselves. That ability is great for repairing the body but in the case of cancer stem cells, it is thought to be responsible for the uncontrolled, lethal growth of tumors.

Both stem cells and cancer stem cells rely on special cellular neighborhoods, or “niches”, to support their function. Outside of those niches, the cells don’t survive well. But cancer stem cells somehow overcome this barrier which allows them to spread and do damage to whole organs.

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Brain MRI showing glioblastoma tumor
Image: Wikimedia Commons

A study this week at The University of Texas MD Anderson Cancer Center zeroed in on the gene QK1 that, when deleted in mice, provides cancer stem cells in the brain the ability to thrive outside their niches.  They team also showed that the loss of the gene slowed a cell process called endocytosis, which normally acts to break down and recycle protein receptors on the cell surface. Those receptors are critical for the cancer stem cell’s self-renew function. So by blocking endocytosis, the gene deletion leads to an accumulation of receptors on the cell surface and in turn that boosts the cancer stem cells’ ability to divide and grow outside of its niche.

In a university press release picked up by Science Daily, team lead Jian Hu talked about exploiting this result to find new ways to defeat glioblastoma, the deadliest form of brain cancer:

“This study may lead to cancer therapeutic opportunities by targeting the mechanisms involved in maintaining cancer stem cells. Although loss of QKI allows glioma stem cells to thrive, it also renders certain vulnerabilities to the cancer cells. We hope to design new therapies to target these.”

CIRM-funded scientists uncover mystery of bone growth in the heart
Calcium helps keep our bones strong but a build-up of the mineral in our soft tissues, like the heart, is nothing but bad news for our health. The origins of this abnormal process called ectopic calcification have been a mystery to scientists because the cells responsible for forming bone and secreting calcium, called osteoblasts, are not found in the heart. So where is the calcium coming from?

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Bone-forming osteoblasts. They’re bad news when found in the heart.
Image: Amgen

This week, a CIRM-funded team at UCLA found the answer: cardiac fibroblasts. The researchers suspected that this most abundant cell in the heart was the culprit behind ectopic calcification. So, using some genetic engineering tricks, they were able to track cardiac fibroblasts with a red fluorescent tag inside mice after a heart injury.

Within a week or so after injury, the team observed that cardiac fibroblasts had clustered around the areas of calcium deposits in the heart. It turns out that those cardiac fibroblasts had taken on the properties of heart stem cells and then became bone-forming osteoblasts. To prove this finding, they took some of those cells and transplanted them into healthy mice. Sure enough, the injection sites where the cells were located began to accumulate calcium deposits.

A comparison of gene activity in these abnormal cells versus healthy cells identified a protein called EPPN1 whose levels were really elevated when these calcium deposits occurred. Blocking EPPN1 put a stop to the calcification in the heart. In a university press release, lead author Arjun Deb explained that this detective work may lead to long sought after therapies:

Everyone recognizes that calcification of the heart and blood vessels and kidneys is abnormal, but we haven’t had a single drug that can slow down or reverse calcification; our study points to some therapeutic targets.

Stem cell stories that caught our eye: Amy Schumer’s MS fundraising; healing traumatic brain injury; schizophrenia iPS insights

Amy Schumer and Paul Shaffer raise money for MS. (Karen Ring)
Two famous individuals, one a comedian/movie star, the other a well-known musician, have combined forces to raise money for an important cause. Amy Schumer and Paul Shaffer have pledged to raise $2.5 million dollars to help support research into multiple sclerosis (MS). This disease affects the nerve cells in both the brain and spinal cord. It eats away at the protective myelin sheaths that coat and protect nerve cells and allow them to relay signals between the brain and the rest of the body. As a result, patients experience a wide range of symptoms including physical, mental and psychiatric problems.

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Comedian Amy Schumer and her Dad who has MS.
(National MS Society)

The jury is still out on the exact cause of MS and there is no cure available. But the Tisch MS Research Center of New York is trying to change that. It is “dedicated to finding the cause and cure for MS” and recently announced, at its annual Future Without MS Gala, that it has pledged to raise $10 million to fund the stem cell research efforts ongoing at the Center. Currently, Tisch is “the only center with an FDA approved stem cell clinical trial for MS in the United States.” You can read more about this clinical trial, which is transplanting mesenchymal stem cell-derived brain progenitor cells into the spinal cord, on the Tisch website.

At the gala, both Amy Schumer and Paul Shaffer were present to show their support for MS research. In an interview with People magazine, Amy revealed that her father struggles with MS. She explained, “Some days he’s really good and he’s with it and we’re joking around. And some days I go to visit my dad and it’s so painful. I can’t believe it.” Her experience watching her dad battle with MS inspired her to write and star in the movie TRAINWRECK, and also to get involved in supporting MS research. “If I can help at all I’m gonna try, even if that means I’ll get hurt,” she said.

Stem cells may help traumatic brain injuries (Kevin McCormack
Traumatic brain injury (TBI) is a huge problem in the US. According to the Centers for Disease Control and Prevention around 1.7 million Americans suffer a TBI every year; 250,000 of those are serious enough to result in a hospitalization; 52,000 are fatal. Even those who survive a TBI are often left with permanent disabilities, caused by swelling in the brain that destroys brain cells.

Now researchers at the University of Texas Health Science Center at Houston say using a person’s own stem cells could help reduce the severity of a TBI.

The study, published in the journal Stem Cells, found that taking stem cells from a person’s own bone marrow and then re-infusing them into the bloodstream, within 48 hours of the injury, can help reduce the swelling and inflammation that damages the brain.

In an interview with the Houston Chronicle Charles Cox, the lead researcher – and a member of CIRM’s Grants Working Group panel of experts – says the results are not a cure but they are encouraging:

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Charles Cox
(Drew Donovan / UTHealth)

“I’m talking about the difference between someone who recovers to the point that they can take care of themselves, and someone who is totally dependent on someone else for even simple tasks, like using the bathroom and bathing. That’s a dramatic difference.”

Schizophrenia: an imbalance of brain cell types?

Schizophrenia is a chronic mental disorder with a wide range of disabling symptoms such as delusional thoughts, hearing voices, anxiety and an inability to experience pleasure. It’s estimated that half of those with schizophrenia abuse drugs and alcohol, which likely contributes to increased incidence of unemployment, homelessness and suicide. No cure exists for the disorder because scientists don’t fully understand what causes it, and available treatments only mask the symptoms.

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A patient’s artistic representation of living with schizophrenia
(Wikipedia)

This week, researchers at the RIKEN Brain Science Institute in Japan reported new clues about what goes wrong at a cellular and molecular level in the brains of people with schizophrenia. The scientists created induced pluripotent stem cells (iPSCs) from healthy donors, as well as patients with schizophrenia, and then changed or specialized them into nerve cells, or neurons. They found that fewer iPSCs developed into neurons when comparing the cells from people with schizophrenia to the healthy donor cells. Instead, more iPSCs specialized into astrocytes, another type of brain cell. This fewer neurons/more astrocytes shift was also seen in brains of deceased donors who had schizophrenia.

Looking inside the cells, the researchers found higher levels of a protein called p38 in the neurons derived from the people with schizophrenia. Inhibiting the activity of p38 led to increased number of neurons and fewer astrocytes, which resembles the healthy state. These results, published in Translational Psychiatry and picked up by Health Canal, point to inhibitors of p38 activity as a potential path for developing new treatments.

Stem cell stories that caught our eye: How Zika may impact adult brains; Move over CRISPR there’s a new kid in town; How our bodies store fat

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

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Zika mosquito

Zika virus could impact adult brains

It’s not just a baby’s developing brain that is vulnerable to the Zika virus, adult brains may be too. A new study shows that some stem cells that help repair damage in the adult brain can be impacted by Zika. This is the first time we’ve had any indication this could be a problem in a fully developed brain.

The study, in the journal Cell Stem Cell, looked at neural progenitors, a  stem cell that plays an important role in helping replace or repair damaged neurons, or nerve cells, in the brain. The researchers exposed the cells to the Zika virus and found that it infected the cells, causing some of the cells to die, and also limited the ability of the cells to proliferate.

In an interview in Healthday, Sujan Shresta, a researcher at the La Jolla Institute for Allergy and Immunology and one of the lead authors of the study, says although their work was done in adult mice, it may have implications for people:

“Zika can clearly enter the brains of adults and can wreak havoc. But it’s a complex disease, it’s catastrophic for early brain development, yet the majority of adults who are infected with Zika rarely show detectable symptoms. Its effect on the adult brain may be more subtle and now we know what to look for.”

Move over CRISPR, there’s a new gene-editing tool in town

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Jennifer Lopez: Photo courtesy MTV

For much of the last year the hottest topic in stem cell and gene editing research has been CRISPR and the ease with which it can be used to edit genes. It’s so hot that apparently it’s the title of an upcoming TV show starring Jeniffer Lopez.

But hold on J-Lo, a new study in Nature Communications says by the time the show is on the air it may be old hat. Researchers at Carnegie Mellon and Yale University have developed a new gene-editing system, one they claim is easier to use and more accurate than CRISPR. And to prove it, they say they have successfully cured a genetic blood disorder in mice, using a simple IV approach.

Tools like CRISPR use enzymes to cut open sections of DNA to edit a specific gene. It’s like using a pair of scissors to cut a piece of string that has a big knot in the middle; you cut out the knot then join the ends of the string together. The problem with CRISPR is that the enzymes it uses are quite large and hard to use in a living animal – let alone a human – so they have to remove the target cells from the body and do the editing in the lab. Another problem is that CRISPR sometimes cuts sections of DNA that the researchers don’t want cut and could lead to dangerous side effects.

Greater precision

The Carnegie Mellon/Yale team say their new method avoids both problems. They use nanoparticles that contain molecules made from peptide nucleic acid (PNA), a kind of artificial form of DNA. This PNA is engineered to be able to cut open DNA and bind to a specific target without cutting anything else.

The team used this approach to target the mutated gene in beta thalassemia, a blood disorder that can be fatal if left untreated. The therapy binds to the malfunctioning gene, enabling the body’s own DNA repair system to correct the problem.

In a news story in Science Daily Danith Ly, one of the lead authors on the study, says even though the technique was successful in editing the target genes just 7 percent of the time, that is way more than the 0.1 percent rate most other gene editing tools achieve.

“The effect may only be 7 percent, but that’s curative. In the case of this particular disease model, you don’t need a lot of correction. You don’t need 100 percent to see the phenotype return to normal.”

Hormone that controls if and when fat cells mature

Obesity is one of the fastest growing public health problems in the US and globally. Understanding the mechanisms behind how that happens could be key to finding ways to address it. Now researchers at Stanford University think they may have uncovered an important part of the answer.

Their findings, reported in Science Signaling, show that mature fat cells produce a hormone called Adamts1 which acts like a switch for surrounding stem cells, determining if they change into fat-storing cells.   People who eat a high-fat diet experience a change in their Adamst1 production, and that triggers the nearby stem cells to specialize and start storing fat.

There are still a lot of questions to be answered about Adamst1, including whether it acts alone or in conjunction with other as yet unknown hormones. But in an article in Health Canal, Brian Feldman, the senior author of the study, says they can now start looking at potential use of Adamst1 to fight obesity.

“That won’t be a simple answer. If you block fat formation, extra calories have to go somewhere in the body, and sending them somewhere else outside fat cells could be more detrimental to metabolism. We know from other researchers’ work that liver and muscle are both bad places to store fat, for example. We do think there are going to be opportunities for new treatments based on our discoveries, but not by simply blocking fat formation alone.”

 

Stem cell stories that caught our eye: Blood stem cells on a diet, Bladder control after spinal cord injuries, new ALS insights

Putting blood stem cells on a diet. (Karen Ring)

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Valine. Image: BMRB

Scientists from Stanford and the University of Tokyo have figured out a new way to potentially make bone marrow transplants more safe. Published yesterday in the journal Science, the teams discovered that removing an essential amino acid, called valine, from the diets of mice depleted their blood stem cells and made it easier for them to receive bone marrow transplants from other mice without the need for radiation or chemotherapy. Removing valine from human blood stem cells yielded similar results suggesting that this therapeutic approach could potentially change and improve the way that certain cancer patients are treated.

In an interview with Science Magazine, senior author Satoshi Yamazaki explained how current bone marrow transplants are toxic to patients and that an alternative, safer form of treatment is needed.

“Bone marrow transplantation is a toxic therapy. We have to do it to treat diseases that would otherwise be fatal, but the quality of life afterward is often not good. Relative to chemotherapy or radiation, the toxicity of a diet deficient in valine seems to be much, much lower. Mice that have been irradiated look terrible. They can’t have babies and live for less than a year. But mice given a diet deficient in valine can have babies and will live a normal life span after transplantation.”

The scientists found that the effects of a valine-deficient diet were mostly specific to blood stem cells in the mice, but also did affect hair stem cells and some T cells. The effects on these other populations of cells were not as dramatic however as the effects on blood stem cells.

Going forward, the teams are interested to find out whether valine deficiency will be a useful treatment for leukemia stem cells, which are stem cells that give rise to a type of blood cancer. As mentioned before, this alternative form of treatment would be very valuable for certain cancer patients in comparison to the current regimen of radiation treatment before bone marrow transplantation.

Easing pain and improving bladder control in spinal cord injury (Kevin McCormack)
When most people think of spinal cord injuries (SCI) they focus on the inability to walk. But for people with those injuries there are many other complications such as intense nerve or neuropathic pain, and inability to control their bladder. A CIRM-funded study from researchers at UCSF may help point at a new way of addressing those problems.

The study, published in the journal Cell Stem Cell, zeroed in on the loss in people with SCI of a particular amino acid called GABA, which acts as a neurotransmitter in the central nervous system and inhibits nerve transmission in the brain, calming nervous activity.

Here’s where we move into alphabet soup, but stick with me. Previous studies showed that using cells called inhibitory interneuron precursors from the medial ganglionic eminence (MGE) helped boost GABA signaling in the brain and spinal cord. So the researchers turned some human embryonic stem cells (hESCs) into MGEs and transplanted those into the spinal cords of mice with SCI.

Six months after transplantation those cells had integrated into the mice’s spinal cord, and the mice not only showed improved bladder function but they also seemed to have less pain.

Now, it’s a long way from mice to men, and there’s a lot of work that has to be done to ensure that this is safe to try in people, but the researchers conclude: “Our findings, therefore, may have implications for the treatment of chronically spinal cord-injured patients.”

CIRM-funded study reveals potential new ALS drug target (Todd Dubnicoff)
Of the many diseases CIRM-funded researchers are tackling, Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s Disease, has got to be one of the worst.

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Motor neurons derived from skin cells of a healthy donor
Image: UC San Diego

This neurodegenerative disorder attacks and kills motor neurons, the nerve cells that control voluntary muscle movement. People diagnosed with ALS, gradually lose the ability to move their limbs, to swallow and even to breathe. The disease is always fatal and people usually die within 3 to 5 years after initial diagnosis. There’s no cure for ALS mainly because scientists are still struggling to fully understand what causes it.

Stem cell-derived “disease in a dish” experiments have recently provided many insights into the underlying biology of ALS. In these studies, skin cells from ALS patients are reprogrammed into an embryonic stem cell-like state called induced pluripotent stem cells (iPSCS). These iPS cells are grown in petri dishes and then specialized into motor neurons, allowing researchers to carefully look for any defects in the cells.

This week, a UC San Diego research team using this disease in a dish strategy reported they had uncovered a cellular process that goes haywire in ALS cells. The researchers generated motor neurons from iPS cells that had been derived from the skin samples of ALS patients with hereditary forms of the disease as well as samples from healthy donors. The team then compared the activity of thousands of genes between the ALS and healthy motor neurons. They found that a particular hereditary mutation doesn’t just impair a protein called hnRNP A2/B1, it actually gives the protein new toxic activities that kill off the motor neurons.

Fernando Martinez, the first author on this study in Neuron, told the UC San Diego Health newsroom that these news results reveal an important context for their on-going development of therapeutics that target proteins like hnRNP:

“These … therapies [targeting hnRNP] can eliminate toxic proteins and treat disease. But this strategy is only viable if the proteins have gained new toxic functions through mutation, as we found here for hnRNP A2/B1 in these ALS cases.”

Stem cell stories that caught our eye: relief for jaw pain, vitamins for iPSCs and Alzheimer’s insights

Jaw bone stem cells may offer relief for suffers of painful joint disorder
An estimated 10 million people in the US – mostly women –  suffer from problems with their temporomandibular joint (TMJ) which sits between the jaw bone and skull. TMJ disorders can lead to a number of symptoms such as intense pain in the jaw, face and head; difficulty swallowing and talking; and dizziness.

ds00355_im00012_mcdc7_tmj_jpgThe TMJ is made up of fibrocartilage which, when healthy, acts as a cushion to enable a person to move their jaw smoothly. But this cartilage doesn’t have the capacity to heal or regenerate so treatments including surgery and pain killers only mask the symptoms without fixing the underlying damage of the joint.

Reporting this week in Nature Communications, researchers at Columbia University’s College of Dental Medicine identified stem cells within the TMJ that can form cartilage and bone – in cell culture studies as well as in animals. The research team further showed that the signaling activity of a protein called Wnt leads to a reduction of these fibrocartilage stem cells (FSCSs) in animals and as a result causes deterioration of cartilage. But injecting a known inhibitor of Wnt into the animals’ damaged TMJ spurred growth and healing of the joint.

The team is now in search of other Wnt inhibitors that could be used in a clinical setting. In a university press release, Jeremy Mao, a co-author on the paper, talked about the implications of these results:

“They suggest that molecular signals that govern stem cells may have therapeutic applications for cartilage and bone regeneration. Cartilage and certain bone defects are notoriously difficult to heal.”

Take your vitamins: good advice for people and iPS cells
From a young age, we’re repeatedly told how getting enough vitamins each day is important for a healthy life. Our bodies don’t produce these naturally occurring chemicals but they carry out critical biochemical activities to keep our cells and organs functioning properly.

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Carrots: a great source of vitamin A. Image source: Wikimedia Commons

Well, it turns out that vitamins are also an important ingredient in stem cell research labs. Results published the Proceedings of the National Academy of Sciences (PNAS) this week by scientists in the UK and New Zealand show that vitamin A and C work together synergistically to improve the efficiency of reprogramming adult cells, like skin or blood, into the embryonic stem cell-like state of induced pluripotent stem cells (iPSCs).

By the time a stem cell has specialized into, let’s say, a skin cell, only skin cell-specific genes are active while others genes, like those needed for liver function, are shut down. Those non-skin genes are silenced through the attachment of chemical tags on the DNA, a process called methylation. It essentially provides the DNA with the means of maintaining a skin cell “memory”. To convert a skin cell back into a stem cell-like state, researchers in the lab must erase this “memory” by adding factors which demethylate, or remove the methylation tags on the silenced, non-skin related genes.

In the current research picked up by Science Daily, the researchers found that both vitamin A and C increase demethylation but in different ways. The study showed that vitamin A acts to increase the production of proteins that are important for demethylation while vitamin C acts to enhance the enzymatic activity of demethylation.

These insights may help add to the growing knowledge on how to most efficiently reprogram adult cells into iPSCs. And they may prove useful for a better understanding of certain cancers which contain cells that are essentially reprogrammed into a stem cell-like state.

New angles for dealing with the tangles in the Alzheimer’s brain
The memory loss and overall degradation of brain function seen in people with Alzheimer’s Disease (AD) is thought to be caused by the accumulation of amyloid and tau proteins which form plaques and tangles in the brain. These abnormal structures are toxic to brain cells and ultimately lead to cell death.

But other studies of post-mortem AD brains suggest a malfunction in endocytosis – a process of taking up and transporting proteins to different parts of the cell – may also play a role. While follow up studies corroborated this initial observation, they didn’t look at endocytosis in nerve cells so it remained unclear how much of a role it played in AD.

In a CIRM-funded study published this week in Cell Reports, UC San Diego researchers made nerve cells from human iPSCs and used the popular CRISPR and TALEN gene editing techniques to generate mutations seen in inherited forms of AD. One of those inherited mutations is in the PS1 gene which has been shown to play a role in transporting amyloid proteins in nerve cells. The research confirmed that this mutation as well as a mutation in the amyloid precursor protein (APP) led to a breakdown in the proper trafficking of APP within the mutated nerve cells. In fact, they found an accumulation of APP in a wrong area of the nerve cell. However, blocking the action of a protein called secretase that normally processes the APP protein helped restore proper protein transport. In a university press release, team leader Larry Goldstein, explained the importance of these findings:

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Larry Goldstein.
Image: UCSD

“Our results further illuminate the complex processes involved in the degradation and decline of neurons, which is, of course, the essential characteristic and cause of AD. But beyond that, they point to a new target and therapy for a condition that currently has no proven treatment or cure.”

 

 

Stem cell stories that caught our eye: Designer bags from human skin, large-scale stem cell production, new look at fat stem cells

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Designer bags from human skin? I had to share a bizarre story I read this week about a UK fashion designer who is making a collection of luxury handbags from lab-grown human skin called Pure Human. What’s even weirder is that the human skin used was engineered to contain the genetic material or DNA of the famous fashion designer Alexander McQueen who passed away in 2010.

A prototype bag, made with pig skin, from Tina Gorjanc’s Pure Human collection (Credit: Tina Gorjanc)

A prototype bag, made with pig skin, from Tina Gorjanc’s Pure Human collection (Credit: Tina Gorjanc & Signals blog for caption)

I had to admit I cringed when I first read about it in CCRM’s Signals Blog, but now I am fascinated that someone is actually doing this and intrigued about the ethical conversations that this story will undoubtedly stir up.

While it isn’t possible to patent a person’s DNA, it is possible to patent a technology that uses human DNA and products made from that technology. According to Signals, “the aim of the collection is to highlight existing legal loopholes around ownership of a person’s DNA and to open the doors for tissue bioengineering into the world of fashion.”

The collection’s designer, Tina Gorjanc, explained her motivation behind Pure Human:

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Tina Gorjanc

“My main goal was to show that it is possible to patent a process using human genetic information in a domain other than medicine. Biotechnology is happening at a really rapid pace and legislation has not kept up with it.”

 

She also sees her bags as an untapped resource in the global luxury goods market which is now apparently worth $1 trillion dollars.

“When it comes to bioengineering, people tend to skip the luxury goods market because they think it’s too shallow and not important, but if you look at it, it’s one of the biggest markets that we have – and one that is open to new technology.”

Imagine having the option to bypass animal leather products for engineered human skin-based products? But on the flip side, the author of the Signals blog, Jovana Drinjakovic, makes a great point at the end of her piece by saying: just because we can do this, does it mean we should?

Drinjakovic finishes her piece with a reality-check quote from Dr. Marc Jeschke, the leader of a burn research and skin regeneration lab in Toronto:

“We are trying to find a way to make skin that is functional and won’t be rejected after a transplant. But just to grow skin for fashion – I don’t think that’s very useful.”

 

Large-Scale Stem Cell Production in Texas. A nonprofit company in San Antonio, Texas, called BioBridge, has big plans to produce large amounts of clinical-grade stem cells for regenerative medicine purposes. The company recently received $7.8 million in funding from the Medical Technology Enterprise Consortium to pursue this effort.

BioBridge will work with GenCure, a subsidiary company, to develop the technology to manufacture different types of stem cells at a large scale. These stem cells will be clinical-grade, meaning that they can be used for cell therapy applications in patients. BioBridge’s goal is to provide enough stem cells for both academic researchers and companies who need more than their current lab resources can generate.

The CEO of GenCure, Becky Cap, explained the need for this type of large-scale stem cell manufacturing technology in an interview with Xconomy:

“The capabilities in this sector right now are at a scale that’s appropriate for bench research and some clinical research, depending on the indication and volume of cells we need. We’re talking about moving from hundreds of millions of cells to billions of cells. You need billions of cells to do tissue regeneration and scaffold reengineering.”

Two other companies with expertise in cell manufacturing, StemBioSys from San Antonio and RoosterBio in Maryland, will be working with BioBridge and GenCure over the next three years on specific projects. StemBioSys plans to develop materials that will be used to promote stem cell growth. RoosterBio will take stem cell culturing from small-scale petri dishes to large-scale bioreactors that can produce billions of cells.

It will be interesting to see how the BioBridge collaboration works out. Xconomy concluded:

“This sort of large-scale manufacturing is still years out. The results that come from the work will be incorporated into a contract manufacturing operation that BioBridge is opening within GenCure.”

 

A new way to look at fat stem cells. (By Todd Dubnicoff)

Human fat stem cells, scientifically known as human adipose stem cells (hASC), are an attractive cell source for regenerative medicine. Their low tendency to cause tissue rejection and their ability to transform into bone cells make them particularly well-suited for developing cell-based treatments for osteoporosis, a disease that weakens bones and makes them susceptible to fractures. And thanks to the numerous liposuction procedures performed in the U.S. each year, hASCs are readily available to researchers.

Electron microscope image showing the eroded, inner structure of a back bone in an 89 year old woman with osteoposis. Image courtesy the Bone Research Society

Electron microscope image showing the eroded, inner structure of a back bone in an 89 year old woman with osteoposis. Image courtesy the Bone Research Society.

But a lingering problem with hASCs as a reliable cell source for future therapies is their extreme patient-to-patient variability. Studies have shown that all sorts of factors like gender, body mass index (BMI) and age can have profound effects on the ability of hASCs to multiply and to specialize into bone cells.

Now, University of Missouri researchers describe the novel use of a measuring device to make more quantitative comparisons of different sets of donor hASCs. The instrument, called an electrical cell-substrate impedance spectroscopy (ECIS) – try saying that three times fast! – sends a very weak, noninvasive current through the cells and can measure changes in the cells’ shape in real-time. Other studies had shown that ECIS can quantitatively detect differences between hASCs and human bone marrow-derived mesenchymal stem cells as they mature into their respective cell types.

In the current Stem Cells Translational Medicine study, picked up this week by Health Canal, hASCs were obtained from young (24–36 years old), middle-aged (48–55 years old), and elderly (60–81 years old) donors. The ECIS results showed that stem cells from older donors matured into bone cells much quicker (~ 1day) than the younger cell of cells (~10 day). You might have intuitively thought the youngest stem cells would mature the fastest. But the end result of the difference is that the young set of stem cells multiplied much more than the cells from older donor and they accumulated more calcium over time.

This noninvasive, quantitative tool for predicting a fat stem cell’s potential to specialize into bone has the promise to improve quality control for manufacturing cell therapies, and it also provides researchers a means to better observe the underlying biological basis for this patient-to-patient variability in human fat cells.

Stem cell stories that caught our eye: healing diabetic ulcers, new spinal cord injury insights & an expanding CRISPR toolbox

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Stem cells heal diabetic foot ulcers in pilot study
Foot ulcers are one of the many long-term complications that diabetics face. About 15 percent of patients develop these open sores which typically appear at the bottom of the foot. In a quarter of these cases, the ulcers lead to serious infection requiring amputation.

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Diabetic foot ulcers are open sores that don’t heal and in many cases leads to amputation. Image source: Izunpharma

But help may be on the horizon in the form of stem cells. Researchers at Mansoura University in Egypt recently presented results of a small study in which 10 patients with diabetic foot ulcers received standard care and another 10 patients received standard care plus injections of mesenchymal stem cells that had been collected from each patient’s own bone marrow. After just six weeks, the stem cell treated group showed a 50% reduction in the foot ulcers while the group with only standard care had a mere 7% reduction.

These superior results with the stem cells were observed even though the group receiving the stem cells had larger foot ulcers to begin with compared to the untreated patients. There are many examples of mesenchymal stem cells’ healing power which make them an extremely popular cell source for hundreds of on-going clinical trials. Mesenchymal stem cells are known to reduce inflammation and increase blood vessel formation, two properties that may be at work to give diabetic foot ulcers the chance to get better.

Medscape Medical News reported on these results which were presented at the 2016 annual meeting of the European Association for the Study of Diabetes (EASD) 2016 Annual Meeting

Suppressing nerve signals to help spinal cord injury victims
Losing the use of one’s limbs is a profound life-altering change for spinal cord injury victims. But their quality of life also suffers tremendously from the loss of bladder control and chronic pain sensations. So much so, victims often say that just improving these secondary symptoms would make a huge improvement in their lives.

While current stem cell-based clinical trials, like the CIRM-funded Asterias study, aim to reverse paralysis by restoring loss nerve signals, recent CIRM-funded animal data published in Cell Stem Cell from UC San Francisco suggest that nerve cells that naturally suppress nerve signals may be helpful for these other symptoms of spinal cord injury.

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Mature inhibitory neuron derived from human embryonic stem cells is shown after successfully migrated and integrated into the injured mouse spinal cord.
Photo by Jiadong Chen, UCSF

It turns out that the bladder control loss and chronic pain may be due to overactive nerve signals. So the lab of Arnold Kriegstein transplanted inhibitory nerve cells – derived from human embryonic stem cells – into mice with spinal cord injuries. The scientists observed that these human inhibitory nerve cells, or interneurons, successfully made working connections in the damaged mouse spinal cords. The rewiring introduced by these interneurons also led to reduced pain behaviors in the mice as well as improvements in bladder control.

 

 

In a Yahoo Finance interview, Kreigstein told reporters he’s eager to push forward with these intriguing results:

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Arnold Kriegstein, UCSF

“As a clinician, I’m very aware of the urgency that’s felt among patients who are often very desperate for treatment. As a result, we’re very interested in accelerating this work toward clinical trials as soon as possible, but there are many steps along the way. We have to demonstrate that this is safe, as well as replicating it in other animals. This involves scaling up the production of these human interneurons in a way that would be compatible with a clinical product.”

 

Expanding the CRISPR toolbox
If science had a fashion week, the relatively new gene editing technology called CRISPR/Cas9 would be sure to dominate the runway. You can think of CRISPR/Cas9 as a protein and RNA complex that acts as a molecular scissor which directly targets and cuts specific sequences of DNA in the human genome. Scientists are using CRISPR/Cas9 to develop innovative biomedical techniques such as removing disease-causing mutations in stem cells in hopes of developing potential treatments for patients suffering from diseases that have no cures.

What’s particularly interesting about the CRISPR/Cas9 system is that the Cas9 protein responsible for cutting DNA is part of a family of CRISPR associated proteins (Cas) that have similar but slightly different functions. Scientists are currently expanding the CRISPR toolbox by exploring the functions of other CRISPR associated proteins for gene editing applications.

A CIRM-funded team at UC Berkeley is particularly interested in a CRISPR protein called C2c2, which is different from Cas9 in that it targets and cuts RNA rather than DNA. Led by Berkeley professor Jennifer Doudna, the team discovered that the CRISPR/C2c2 complex has not just one, but two, distinct ways that it cuts RNA. Their findings were published this week in the journal Nature.

The first way involves creation: C2c2 helps make the guide RNAs that are used to find the RNA molecules that it wants to cut. The second way involves destruction: after the CRISPR/C2c2 complex finds it’s RNAs of choice, C2c2 can then cut and destroy the RNAs.

Doudna commented on the potential applications for this newly added CRISPR tool in a Berkeley News release:

Jennifer-Doudna

Jennifer Doudna: Photo courtesy of iPSCell.com

“This study expands our molecular understanding of C2c2 to guide RNA processing and provides the first application of this novel RNase. C2c2 is essentially a self-arming sentinel that attacks all RNAs upon detecting its target. This activity can be harnessed as an auto-amplifying detector that may be useful as a low-cost diagnostic.”

 

Stem cell stories that caught our eye: two studies of the heart and cool stem cell art

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Image from Scope Blog.

Image from Scope Blog.

Understanding Heart Defects. Healthy heart tissue is made up of smooth, solid muscle, which is essential for normal heart function. Patients with a heart defect called left ventricular non-compaction (LVNC), lack normal heart tissue in their left ventricle – the largest, strongest blood-pumping chamber – and instead have spongy-looking tissue.

LVNC occurs during early heart development where pieces of heart muscle fail to condense (compact) and instead form an airy, sponge-like network that can leave patients at risk for heart failure and other complications.

A team at Stanford is interested in learning how LVNC occurs in humans, and they’re using human stem cells for the answer. Led by CIRM grantee Joe Wu, the scientists generated induced pluripotent stem cells (iPSCs) from four patients with LVNC. iPSCs are cells that can be turned into any other cell in the body, so Wu turned these cells into iPSC-derived heart muscle in a dish.

Wu’s team was particularly interested in determining why some LVNC patients have symptoms of disease while others seem perfectly normal. After studying the heart muscle cells derived from the four LVNC patients, they identified a genetic mutation in a gene called TBX20. This gene produces a type of protein called a cardiac transcription factor, which controls the expression of other heart related genes.

Upon further exploration, the scientists found that the genetic mutation in TBX20 prevented LVNC heart muscle cells from dividing at their normal rate. If they blocked the signal of mutant TBX20, the heart cells went back to their normal activity and created healthy looking heart tissue.

This study was published in Nature Cell Biology and covered by the Stanford Medicine Scope blog. In an interview with Scope, Joe Wu highlighted the big picture of their work:

Joseph Wu Stanford

Joseph Wu Stanford

“This study shows the feasibility of modeling such developmental defects using human tissue-specific cells, rather than relying on animal cells or animal models. It opens up an exciting new avenue for research into congenital heart disease that could help literally the youngest — in utero — patients.”

Stem Cell Heart Patch. Scientists from the University of Wisconsin, Madison are creating stem cell-based heart patches that they hope one day could be used to treat heart disease.

In a collaboration with Duke and the University of Alabama at Birmingham, they’re developing 3D stem cell-derived patches that contain the three main cell types found in the heart: cardiomyocytes (heart muscle cells), fibroblasts (support cells), and endothelial cells (cells that line the insides of blood vessels). These patches would be transplanted into heart disease patients to replace damaged heart tissue and improve heart function.

As with all research that has the potential for reaching human patients, the scientists must first determine whether the heart patches are safe in animal models. They plan to transplant the heart patches into a pig model – chosen because pigs have similar sized hearts compared to humans.

In a UW-Madison News release, the director of the UW-Madison Stem Cell and Regenerative Medicine Center Timothy Kamp, hinted at the potential for this technology to reach the clinic.

“The excitement here is we’re moving closer to patient applications. We’re at a stage when we need to see how these cells do in a large animal heart attack model. We’ll be making patches of heart muscle that can be applied to these injured areas.”

Kamp and his team still have a lot of work to do to perfect their heart patch technology, but they are thinking ahead. Two issues that they are trying to address are how to prevent a patient’s immune system from rejecting the heart patch transplant, and how to make sure the heart patches beat in sync with the heart they are transplanted into.

Check out the heart patches in action in this video:

(Video courtesy of Xiaojun Lian)

Cool Stem Cell Art! When I was a scientist, I worked with stem cells all the time. I grew them in cell culture dishes, coaxed them to differentiate into brain cells, and used a technique called immunostaining to take really beautiful, colorful pictures of my final cell products. I took probably thousands of pictures over my PhD and postdoc, but sadly, only a handful of these photos ever made it into journal publications. The rest collected dust either on my hard drive or in my lab notebook.

It’s really too bad that at the time I didn’t know about this awesome stem cell art contest called Cells I See run by the Centre for Commercialization of Regenerative Medicine (CCRM) in Ontario Canada and sponsored by the Stem Cell Network.

The contest “is about the beauty of stem cells and biomaterials, seen directly through the microscope or through the interpretive lens of the artist.” Scientists can submit their most prized stem cell images or art, and the winner receives a cash prize and major science-art street cred.

The submission deadline for this year’s contest was earlier this month, and you can check out the contenders on CCRM’s Facebook page. Even better, you can vote for your favorite image or art by liking the photo. The last date to vote is October 15th and the scientist whose image has the most likes will be the People’s Choice winner. CCRM will also crown a Grand Prize winner at the Till & McCulloch Stem Cell Meeting in October.

I’ll leave you with a few of my favorite photos, but please don’t let this bias your vote =)!

"Icy Astrocytes" by Samantha Yammine

“Icy Astrocytes” by Samantha Yammine (Vote here!)

"Reaching for organoids" by Amy Wong

“Reaching for organoids” by Amy Wong (Vote here!)

"Iris" by Sabiha Hacibekiroglu

“Iris” by Sabiha Hacibekiroglu (Vote here!)

Stem cell stories that caught our eye: 3D mini-lungs, Parkinson’s culprit, Motherless babies!

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Mimicking human air sacs –  a new lab tool for studying respiratory disease
Studying a flat lawn of cells in a petri dish is so old fashioned these days. The current trend is to use stem cells to create mini-organs called organoids that more closely mimic the actual three dimensional structures that you would find in the human body. We’ve written about the creation of mini-brains, livers, pituitary glands and several other organoids. Now, a UCLA research team has added lung organoids to the list.

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3-D bioengineered lung-like tissue (left) resembles adult human lung (right).
Image credit: UCLA Broad Stem Cell Research Center

Reported yesterday in Stem Cells Translational Medicine, the CIRM-funded study describes the technique of nudging lung stem cells, collected from patients’ lung tissue, to self-assemble into 3D structures that resemble air sacs found in the human lung. This technique will surely usher in a better understanding of idiopathic pulmonary fibrosis, a disease that causes scarring of the lungs, leading to shortness of breath and depriving the organs of oxygen. The cause of the disease isn’t known in most cases and, sadly, people usually die within five years of their initial diagnosis.

One of the main challenges in the lab has been reproducing the tale tell scarring seen in this chronic lung disease. When lung cells are taken from pulmonary fibrosis patients and grown as a flat layer, the cells look healthy. But with this novel lung organoid technique, the researchers were able to manipulate the cells to develop the types of scars seen in actual diseased lungs. Better yet, the methodology is very straight-forward, as Dan Wilkinson described in a university press release:

“The technique is very simple. We can make thousands of reproducible pieces of tissue that resemble lung and contain patient-specific cells.”

Now the researchers are in a position to better understand the cellular and molecular basis of the disease and to test out possible treatments that would work best in each individual.

A common thread running through all Parkinson’s cases
The cause of Parkinson’s disease seems straight-forward enough: nerve cells that produce dopamine – a chemical signal that helps generate smooth body movements – progressively die leading to body stiffness, uncontrollable shaking in the limbs and weakened coordination, just to name a few symptoms.

But the underlying genetics of Parkinson’s is anything but simple. Mutations in several genes are associated with family histories of the disease while other mutations in other genes are known to indirectly increase the risk of developing Parkinson’s. These familial forms of Parkinson’s, however, only make up about 15% of all cases; the remaining are so-called sporadic, meaning there’s no obvious family history. So, treating Parkinson’s disease involves treating each of its many forms. But in a CIRM-funded study, published late last week in Cell Stem Cell, Stanford researchers reported on a common thread that appears to run through all forms of Parkinson’s disease.

The team focused on a known mutation in the LRRK2 gene, found in about 1 out of 20 cases of familial Parkinson’s and which pops up in 1 out of 50 cases of sporadic Parkinson’s. The link between LRRK2 and Parkinson’s had not been understood. The Stanford researchers found it plays an important role in the maintenance of mitochondria, structures that produce a cell’s energy needs.

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Oh, not that Miro’. We’re talking about the protein Miro!
(Image: www.joan-miro.net)

When mitochondria become damaged or old they begin spewing out molecules that are toxic to the cell. In response, the cell gobbles up these mitochondria but only after the LRRK protein interacts with and removes a protein called Miro which normally anchors the mitochondria to the cell’s internal structures. The mutated form of LRRK2 doesn’t interact with Miro very well and, as a result, Miro holds on to the toxic mitochondria which in turn are not dismantled as rapidly.

You’d think this mechanism of action would to be specific to the LRRK2-mutant Parkinson’s but to the scientists’ pleasant surprise, it wasn’t. They discovered this result by creating induced pluripotent stem cells from skin samples collected from twenty different subjects:  four healthy subjects; five with the sporadic Parkinson’s; six with familial Parkinson’s from LRRK2 mutations and five with familial patients from other mutations. The iPS cells were grown into dopamine-producing nerve cells, the kind that die off in Parkinson’s disease. With these cells in hand, they observed the impact of intentionally damaging the mitochondria.

As expected, this damage to the nerve cells from the healthy subjects led to the breakdown of Miro which in turn allowed the detachment and degradation of mitochondria. Also as expected, the nerve cells from patients with the LRRK2 mutant showed delays in the release and degradation of mitochondria. But when the team looked at the other Parkinson’s nerve cells not associated with the LRRK2 mutant, they found the same delay in the release of Miro and degradation of mitochondria.

This result points to Miro as a common player in all forms of Parkinson’s. Xinnan Wang, the team’s leader, spoke about the exciting implications of these findings in a university press release:

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Xinnan Wang

“Existing drugs for Parkinson’s largely work by supplying precursors that faltering dopaminergic nerve cells can easily convert to dopamine. But that doesn’t prevent those cells from dying, and once they’ve died you can’t bring them back. Measuring Miro levels in skin fibroblasts from people at risk of Parkinson’s might someday prove beneficial in getting an accurate, early diagnosis. And medicines that lower Miro levels could prove beneficial in treating the disease.” 

A cautionary tale about science communication
What to leave in, what to leave out: it’s the continual dilemma (I must add a fun dilemma) for a science writer. When writing for a general audience, if you describe a research report in too much detail you’re likely to quickly lose your reader. But not adding enough detail can lead the reader to draw conclusions that aren’t accurate. And just a like a game of telephone, as the story is passed along from one source to another, the resulting storyline has little resemblance to the original research.

Research published this week in Nature Communications provides a case in point. Many of news outlets that picked up the research story which involved the successful production of mouse pups from mixing sperm with an novel type of egg cell that had been induced to divide before fertilization. The resulting headlines suggested that scientists had identified an end run around the need for a female’s egg to produce offspring. Based on a quick glance at these condensed summaries of the research report, you’d think motherless babies were just around the corner.

Gretchen Vogel at Science Magazine wrote a terrific autopsy of this news story, describing in five steps how it took on a life of its own. It’s a humorous (I personally LOL’d when I read it) yet serious cautionary tale of how science communication can go awry. I highly recommended the short piece. For a sneak peek, here’s her “five easy steps to create a tabloid science headline”:

  1. vogel_

    Gretchen Vogel

    Take one jargon-filled paper title: “Mice produced by mitotic reprogramming of sperm injected into haploid parthenogenotes

  2. Distill its research into more accessible language. Text of Nature Communications press release: Mouse sperm injected into a modified, inactive embryo can generate healthy offspring, shows a paper in Nature CommunicationsAnd add a lively headline: “Mouse sperm generate viable offspring without fertilization in an egg
  3. Enlist an organization to invite London writers to a press briefing with paper’s authors.
    Headline of Science Media Centre press release: “Making embryos from a non-egg cell
  4. Have same group distribute a laudatory quote from well-known and respected scientist: 
    “[It’s] a technical tour de force.”
  5. Bake for 24 hours and present without additional reporting. Headline in The Telegraph: “Motherless babies possible as scientists create live offspring without need for female egg,” and in The Guardian: “Skin cells might be used instead of eggs to make embryos, scientists say.”