Stem cell stories that caught our eye; creating bone, turning data into sound, cord blood and path of a stem cell star

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.

A better ratio of bone to fat
. Most of us at any age would prefer a little less fat and older folks, particularly ones plagued by the bone loss of osteoporosis, could use a bit more bone. Since both types of tissues come from mesenchymal stem cells (MSCs) a team at the University of Miami decided to look for chemical triggers that tells those stem cells whether to become fat or bone.

They found an enzyme that seems to do just that. In mice that were born with a mutation in the gene for that enzyme they saw increased bone growth, less fat production and a leaner body mass. HealthCanal picked up the university’s press release that quoted the leader of the team Joshua Hare:

“The production of bone could have a profound effect on the quality of life for the aging population.”

He goes on to note that there are many hurdles to cross before this becomes a therapeutic reality, but the current work points to lots of potential.

Path to becoming a star stem cell scientist. D, the city magazine for Dallas, published a lengthy—nearly 4,000-word—feature on Sean Morrison, one of the undisputed leaders of our field. While it starts out talking about his latest role of creating a multi-pronged center for innovation at

Sean Morrison

Sean Morrison

Children’s Medical Center Dallas and UT Southwestern, it spends most of its words on how he got there.

It’s fun reading how someone gets into a field as new as stem cell science and what keeps them in the field. Initially, for him it seems to originate from an immense curiosity about what was not known about the powerful little stem cells.

“Fifteen years ago, there was nothing known at the molecular level about how stem cells replicate. And I really felt it was a fundamental question in biology to understand. It was a question that was central to a lot of important issues, because the ability of stem cells to self-renew is critical to form your tissues throughout development, to maintain your tissues throughout adulthood.”

There is also a good retelling of Morrison’s role in the protracted and hard-fought battle to make embryonic stem cell research legal during his years in Michigan. He started working on the campaign to overturn the ban in 2006 and in 2008 the voters agreed. The article makes a compelling case for something I have advocated for years: scientists need to practice speaking for the public and get out and do it.

Turning stem cell data into sound. Interpreting scientific data through sound, sonification, is a bit trendy now. But the concept is quite old. Think of the Geiger counter and the speed of the click changing based on the level of radiation.

Researchers tend to consider sonification when dealing with large data sets that have some level of repetitive component. Following the differentiation of a large number of stem cells as they mature into different types of tissue could lend itself to the genre and a team at Cardiff University in Scotland reports they have succeeded. In doing just that.

HealthCanal picked up the university’s piece talking about the project. Unfortunately it does a very poor job of explaining how the process actually works. I did find this piece on ocean microbes that describes the concept of sonification of data pretty well.

Cord blood poised for greater use. I get very uncomfortable when friends ask for medical advice around stem cells. I usually try to give a lay of the land that comes short of direct advice. A common question centers on the value of paying the annual storage fees to freeze their baby’s cord blood. To which, I typically say that for current uses the value is marginal, but for the uses that could come in five to 10 years, it could be quite significant.

So, it was not surprising to read a headline on a Scientific American Blog last December reading “Vast Majority of Life-Saving Cord Blood Sits Unused.” But it was also fun to read a well-documented counter point guest blog on the site this morning by our former President, Alan Trounson. He suggested a better headline would be: “Vast Majority of Life-Saving Cord Blood Sits Poised for Discovery.”

He details how cord blood has become a valuable research tool and lists some of the FDA-approved clinical trials that could greatly expand the indication of cord blood therapy. While some of those trials will likely produce negative results, some will succeed and they all will start to show how to turn those frozen vials into a more valuable resource.

Stem cell stories that caught our eye; cystic fibrosis, brain repair and Type 2 diabetes

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.

“Organoids” screen for cystic fibrosis drugs
. Starting with iPS-type stem cells made by reprogramming skin cells from cystic fibrosis (CF) patients a team at the University of Cambridge in the U.K. created mini lungs in a dish. These organoids should provide a great tool for screening drugs to treat the disease.

The researchers pushed the stem cells to go through the early stages of embryo development and then on to become 3-D distal airway tissue, the part of the lung that processes gas exchange. They were able to use a florescent marker to show an aspect of the cells’ function that was different in cells from CF patients and those from normal individuals. When they treated the CF cells with a drug that is being tested in CF patients, they saw the function correct to the normal state.

Bioscience Technology
picked up the university’s press release about the work published in the journal Stem Cells and Development. It quotes the scientist who led the study, Nick Hannon, on the application of the new tool:

“We’re confident this process could be scaled up to enable us to screen tens of thousands of compounds and develop mini-lungs with other diseases such as lung cancer and idiopathic pulmonary fibrosis.”

To repair a brain knock its “pinky” down. A team at the University of California, San Francisco, has discovered a molecule that when it is shut down nerve stem cells can produce a whole lot more nerves. They call the molecule Pnky, named after the cartoon Pinky and the Brain.

Pinky_and_the_Brain_vol1Pkny belongs to a set of molecules known as long noncoding RNAs (lncRNAs), which researchers are finding are more abundant and more important than originally thought. The most familiar RNAs are the intermediary molecules between the DNA in our genes and the proteins that let our cells function. Initially, all the noncoding RNAs were thought to have no function, but in recent years many have been found to have critical roles in determining which genes are active. And Pnky seems to tamp down the activity of nerve stem cells. In a university press release picked up by HealthCanal Daniel Lim, the head researcher explained what happens when they shut down the gene:

“It is remarkable that when you take Pnky away, the stem cells produce many more neurons. These findings suggest that Pnky, and perhaps lncRNAs in general, could eventually have important applications in regenerative medicine and cancer treatment.”

Lim went onto explain the cancer connection. Since Pnky binds to a protein found in brain tumors, it might be involved in regulating the growth of brain tumors. A lot more work needs to happen before that hunch—or the use of Pnky blockers in brain injury—can lead to therapies, but this study certainly paints an intriguing path forward.

Stem cells and Type 2 diabetes. A few teams have succeeded in using stem cells to produce insulin-secreting tissue to correct Type 1 diabetes in animals, but it has been uncertain if the procedure would work for Type 2 diabetes. Type 1 is marked by a lack of insulin production, while resistance to the body’s own insulin, not lack of insulin, is the hallmark of type 2. A team at the University of British Columbia has new data showing stem cell therapy may indeed have a place in treating Type 2.

In mice fed a high fat diet until they developed the symptoms of Type 2 diabetes the stem cell-derived cells did help, but they did not fully correct the metabolism of the mice until they added one of the drugs commonly used to treat diabetes today. The drugs alone, also did not restore normal metabolism, which is often the case with human Type 2 diabetics.

The combination of drugs and cells improved the mice’s sugar metabolism, body weight and insulin sensitivity. The research appeared in the journal Stem Cell Reports and the University’s press release was picked up by several outlets including Fox News.

They transplanted cells from humans and even though the mice were immune suppressed, they took the added measure of protecting the cells in an encapsulation device. They noted that this would be required for use in humans and showing that it worked in mice would speed up any human trials. They also gave a shout out to the clinical trial CIRM funds at Viacyte, noting that since the Food and Drug Administration has already approved use of a similar device by Viacyte, the work might gain more rapid approval.

New understanding of the inner workings of our genetic tool kit should help us make smarter repairs

For young biology students the steps from genes to their function becomes a mantra: DNA makes RNA and RNA makes protein. But it is really not quite that simple. A few different types of RNA act along the path and we are now learning that the structure, or shape, of the individual RNA molecules affects their function.

Which genes succeed in producing their designated protein determines what the cell actually does—what kind of tissue it is and how well it performs the role it is assigned. Switching gene function on and off turns out to be quite complex with players among the molecules that are part of the backbone of DNA as well as the various forms of RNA. We have made great strides in the past decade in understanding the role of those DNA structural components, the so-called epigenetics, but still have major gaps in our understanding of the many roles of RNA.

DNA dogmaWith CIRM-funding, a team headed by Howard Chang at Stanford has gotten around a major hurdle in unlocking this complex issue. Like DNA, RNA is made up of various repeats of four molecules called bases. Prior to Chang’s work researchers could only track the structure of RNA associated with two of those bases. His team modified a commonly used bio-chemical tool called SHAPE to reveal the workings of all four RNA bases in living cells.

The team verified something that is increasingly being shown, static cells frozen in time a lab dish do not necessarily reflect what goes on in living cells. In this study those differences manifest in the structure of the RNA that determines what molecules are next to each other, which impacts their activity. After more than 2 billion measurements of more than 13,000 RNAs in the lab and in living cells, the team quantified those differences and showed how this molecular “folding” changes the function of the various RNAs.

They published the work, for which they used mouse embryonic stem cells, on-line today in Nature. In the closing paragraph of the journal article they speculate on the impact of the new ability to better understand the roles of RNA:

“In the future, viewing the RNA structurome when cells are exposed to different stimuli or genetic perturbations should revolutionize our understanding of gene regulation in biology and medicine.”

Since so many of the research projects that seek to reverse the course of disease try to change the genetic functioning of cells, this new understanding should be able to reduce the number of blind alleys scientist have to go down to get a desired result. It should allow the design of studies based on more logic and less chance, speeding the development of therapies.

Conference provides critical connections between clinical projects and investors

Having a mission like CIRM’s, which calls on us to develop therapies for unmet medical needs, clearly means we cannot sit back and marvel at all the great projects we have in the pipeline. We have to deliver commercial products available to all patients in need. And that cannot be done without additional investors.

The Alliance for Regenerative Medicine (ARM) takes that maxim seriously as well. The international advocacy organization, of which CIRM was a founding member five years ago, will host its third annual RegenMed Investor Day in New York City next Wednesday March 25.
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During the full-day event 32 companies will present their progress to a wide array of investors. Traditional venture capital investors will be represented alongside investors from institutions and multinational pharmaceutical giants.

The day will be rounded out with three panel discussions and two fireside chats with market research analysts, company CEOs and leading clinicians. The fireside chat during lunch will feature CIRM President and CEO Dr. C. Randall Mills who will talk about public-private partnerships making joint investments to bring therapies to patients, and how the revised work plan we call CIRM 2.0 will make it easier for companies to work together with CIRM to advance promising therapies.

Getting just the eleven projects CIRM is funding in clinical trials today through to commercial products will require a broad mix of funding partnerships. With our portfolio and that of the industry as a whole growing rapidly, conferences like this one are critical.

Stem cell stories that caught our eye; drug screening, aging stem cells in brain repair and blood diseases

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.

Heart-on-a-chip used to screen drugs. With CIRM funding, a team at the University of California, Berkeley, has used stem cell technology to create a virtual heart on an inch-long piece of silicon. The cells in that “chip” mimic the physiology of a human heart and have shown that they can accurately show how drugs will impact the heart.
HeartChip4196107801
Starting with iPS-type stem cells made from reprogramming adult cells the researchers grew them into heart muscle that could beat and align in multiple layers with microscopic channels that mimic blood vessels. They tested three drugs currently used to treat heart disease and found the changes seen in the heart-on-a-chip were consistent with what is seen in patients. For example, they tested isoproterenol, a drug used to treat slow heart rate and saw a dramatic increase in heart rate.

But the real value in the silicon-housed heart will be in screening potential new drugs and finding out adverse impacts before taking them into costly human clinical trials. Genetic Engineering & Biotechnology News wrote up the work and quoted a member of the team, Kevin Healy:

“It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market.”

Brain stem cell activity decreases with age. We have known for some time that the adult stem cells that reside in most of our tissues and spend our lives repairing those tissues are less effective as we age. But the stemness of those cells—their ability to regenerate themselves—has not generally been questioned, rather we have assumed they just lost some of their ability to mature into the type of cell needed to make the repair.

Now, a team at the Ludwig-Maximilians-Universitat in Munich has published data suggesting that brain stem cells over time loose both their ability to renew themselves and some of their ability to become certain kinds of nerves. ScienceDaily picked up a press release from the institution and it quoted one of the authors, Magdalena Gotz, on the implications of their finding for therapy.

“In light of the fact that the stem cell supply is limited, we must now also look for ways to promote the self-renewal rate of the stem cells themselves and maintain the supply for a longer time.”

Another alternative for correcting genetic blood disease. CIRM funds a few programs that are trying to treat blood diseases such as sickle cell anemia and beta thalassemia by genetically altering blood forming stem cells. The goal being to correct defects in the gene for hemoglobin, the protein that carries oxygen in red blood cells.

Instead of starting with a patient’s own blood stem cells, which can require a somewhat traumatic harvest procedure, a new approach by a team at the Salk Institute in La Jolla creates iPS type stem cells by reprogramming the cells in a small skin sample. They mature those into blood stem cells and genetically modify them so that they can produce red blood cells that have the correct hemoglobin.

The Salk team uses a modified cold virus to carry the gene into the cell. ScienceDaily picked up the institute’s press release, which quotes one of the co-first authors on the study Mo Li on how the process works:

“It happens naturally, working like a zipper. The good gene just zips in perfectly, pushing the bad one out.”

CIRM funds other work by the senior author, Juan Carlos Izpisua Belmonte, but not this project. Because you never know which technology is going to work out best in the long term, it is nice to see other funders stepping up and pushing this alternative forward.

Pathway discovered that could yield therapies to prevent hearts turning to “bone”

In the Rolling Stones’ lyrics having a “Heart of Stone” protected you from heartbreak. But over a million Americans are developing hearts of bone and it could kill them.

CIRM-funded researchers at the Gladstone Institutes think they have uncovered the path to this destructive hardening of the heart and that could lead to therapies to stop the damage. In particular, they looked at heart valves and why in some people the cells in those valves start acting like bone and produce calcium that causes them to get rigid and loose their proper function.

Valve cells come from a family of cells called endothelial cells that includes the lining of blood vessels, which are also prone to inappropriate production of calcium and hardening. So, the findings could have much broader implication for heart disease and therapy.

A mutation in the Notch1 gene makes cells react inappropriately to the sheer stress caused by blood flow. Team found BMP, SFB and MMP genes control this.

A mutation in the Notch1 gene makes cells react inappropriately to the sheer stress caused by blood flow. Team found BMP, SFB and MMP genes control this.

Led by senior author Deepak Srivastava, the team used stem cell technology to create endothelial cells from patients with genetic calcific aortic valve disease (CAVD) and from normal individuals. They then pushed those cells to mature into valve cells in the lab and monitored which genes were turned on or off during the process, comparing the disease carrying and normal cells.

They built on a previous discovery of Srivastava, who found that a defect in the gene NOTCH1 can cause valve birth defects and CAVD. Searching hundreds of genes and gene switches they came upon three genes that appear to be master regulators of the path that leads cells to overproduce calcium. In a press release from the Gladstone, he said:

“Identifying these master regulators is a big step in treating CAVD, not just in people with the NOTCH1 mutation, but also in other patients who experience calcification in their valves and arteries. Now that we know how calcification happens and what the key nodes are, we know what genes to look for that might be mutated in other related forms of cardiovascular disease.”

The release noted that the research team is now screening for drugs that can act on this gene network. Srivastava’s main focus has been on congenital pediatric heart disease. He discusses that research in three brief videos that include the story of one very special young patient.

Stem cell stories that caught our eye; Parkinson’s, drug boosts stem cells in MS and gender equity in science

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 survive and aid Parkinson’s in monkey.
Ole Isacson, a pioneer in the effort to figure out how to use stem cells to treat Parkinson’s Disease, has published new research that suggests a good option. His Harvard team used nerves grown from reprogrammed iPS type stem cells created from the monkey’s own skin.

Dopamine producing nerves created from skin cells of primates

Dopamine producing nerves created from skin cells of primates

His earlier efforts using nerves grown from embryonic stem cells did not result in production of the dopamine that Parkinson’s patients need. He speculates that this was because they were donor cells and required immune suppression to avoid rejection. With the iPS-derived nerves no immune suppressants were needed and the cells survived two years and reversed much of the Parkinson’s symptoms in the one animal that got that type of cell.

ScienceBlog picked up the university’s press release, which described the therapeutic benefit this way:

Isacson said the conclusion of this experiment marks “the first time that an animal has recovered to the same activity level he had before.” He noted that the animal was “able to move as fast around its home cage” as an animal without Parkinson’s, and had normal agility, though individual motions were still slowed by the disease.

He also cautioned that it would be at least three years before he could do the experiments needed to prove the procedure was safe enough to use in patients.

Nerve cells for memory created from stem cells.
The cerebral cortex is the most complex part of our brains. This large outer layer processes memory, vision and language. Its complexity has always given researcher pause in thinking about ways to use stem cells to repair damage in it. Now, an international team working in Belgium and France has grown cortex nerves in the lab, transplanted them in mice with damaged cortices and seen the nerves survive and integrate into the healthy neighboring tissue.

In these experiments the damaged area in the mice was in the visual cortex and some of the animals did show a return of visual stimulus after the transplants. The researchers published their results in the journal Neuron and Science Daily picked up a release from the Belgium university, Libre de Bruxelles.

Drug gets brain stem cells to do better job. We retain a few brain stem cells throughout our life, but they are often not up to the task of repairing large areas of damage. This is the case in multiple sclerosis when our immune system destroys much of the myelin sheath that coats and protects the nerves.

Using a drug already approved by the Food and Drug Administration for other uses, researchers at the University of Buffalo were able to increase the production of myelin in a mouse model of the disease. The drug targets the middleman cells that are half way between stem cells and mature myelin called oligodendrocyte progenitor cells.

They found the drug by first stepping back to look to see what molecules inside the cell are normally active as the stem cells mature to progenitors and then to myelin. They identified a specific molecular pathway needed for this maturation and then looked for drugs that might impact that pathway. They hit upon solifenacin, an agent used for overactive bladder, which results from activity in that same molecular pathway. They told Genetic Engineering & Biotechnology News that they are now looking for funding to conduct human clinical trails.

Stem cell foundation pushes for gender equality. The New York Stem Cell Foundation launched its “Initiative on Women in Science and Engineering (IWISE)” in February 2014 and this week the journal Cell Stem Cell published the resulting recommendations.

The IWISE working group’s first meeting a year ago resulted in seven actionable strategies to advance women in science, medicine and engineering. The group continued to refine those over the year, met again last month to finalize them prior to publication.

The seven strategies include:
1) Implement flexible family care spending
2) Provide “extra hands” awards
3) Recruit gender-balanced external review committees and speaker selection committees
4) Incorporate implicit bias statements
5) Focus on education as a tool
6) Create an institutional report card for gender equality
7) Partner to expand upon existing searchable databases of women in science, medicine, and engineering

The press release from NYSCF was picked up on the web site ECN and has a quote from former CIRM governing board member, Claire Pomeroy, who is now president of the Lasker Foundation.

“The brain power provided by women in science is essential to sustaining a thriving US society and economy. It is time to move beyond just lamenting its loss and embrace the actions called for in this timely report.”

Stem cell stories that caught our eye; viral genes in embryos, underuse of transplants and joint pain clinics

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.

Ancient viral invaders help make us, us. The cells of our ancestors millions of years ago may have found a way to turn viral invasion into a good thing. This genetic lemons-to-lemonade tale comes from a team in Singapore that meticulously looked at 650,000 bits of virus genes that have been left behind in our cells after viral infections.

Retroviruses like HIV can only replicate by integrating their genes into ours and getting our cellular machinery to make new copies of themselves. Biologists have long known that they often leave behind bits of their genes, but had assumed this became part of the “junk DNA” that does not serve any function and that makes up the bulk of the genetic material in our cells. That scenario has started to change over the past few years as teams have reported examples of those retroviral genetic elements playing a role in the regulation—the turning on and off—of our functional genes.
virus
Jonathan Goke, the lead researcher on the project at the Genome Institute of Singapore, wrote that roughly 1,400 of those viral gene elements were involved in the very early stages of embryo development, helping determine how cells decide to mature into different types of tissue. They seem to be needed for determining who we are.

In an article on the website science 2.0 Goke speculated that these viruses may have been able to speed-up evolution by making changes in gene function faster than random mutation.

Blood stem cell transplants under used. Even as the number of blood stem cell transplants ever performed has passed the one million mark, a new report warns that lives are at risk because too many patients that could benefit are not getting these transplants. Blood stem cell transplants, which started as bone marrow transplants, provide the only shot at life-saving therapy for many patients, mostly those with blood cancers.

An international team, led by Dietger Niederwieser of the University Hospital Leipzig in Germany, found a dramatic under use of donor cells for transplants that varied widely around the world. Writing in the Lancet they reported that just 0.4 people per 10 million in the Philippines get such transplants, but in Israel the number shoots up to 506. The report noted both uneven distribution of resources needed to perform the complex procedure and inconsistent support for and participation in donor registries. Niederwieser was quoted in a press release from the journal picked up by ScienceDaily:

“Patients, many of them children, are facing a life and death situation. Ultimately they will die if they cannot get the treatment they need. All countries need to provide adequate infrastructure for patients and donors to make sure that everyone who needs a transplant gets one, rather than the present situation in which access remains restricted to countries and people with sufficient resources.”

What is real with stem cells and joint pain? Bethesda Magazine, the local publication for the county that is home to the National Institutes of Health (NIH), produced a good piece giving the perspective of patients wanting to avoid joint replacement surgery as well as scientists leery of cell-based procedures that have very little evidence to back them up.

The magazine reached out to its neighbor, the NIH to provide some perspective. It quotes Pamela Robey, the co-coordinator of the NIH Bone Marrow Stromal Cell Transplantation Center—those stromal cells are one type of cell often touted by clinics offering to treat joint pain.

“There are a huge number of clinical trials, but there has been next to no published information. The bottom line is there’s no real rigorous data showing it is actually repairing the joint.”

The author also talked to CIRM grantee Larry Goldstein of the University of California, San Diego, in his role as a member of the Ethics and Public Policy Committee of the International Society for Stem Cell Research. He notes that what clinics are offering is unproven and the author directs readers to the ISSCR web site’s “Closer Look” section to get more information on how to evaluate potential therapies they may be considering.

Stem cell stories that caught our eye; progress toward artificial brain, teeth may help the blind and obesity

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.

More progress toward artificial brain. A team at the RIKEN Institute in Japan has used stem cells in a 3-D culture to create brain tissue more complex than prior efforts and from an area of the brain not produced before, the cerebellum—that lobe at the lower back of the brain that controls motor function and attention. As far back as 2008, a RIKEN team had created simple tissue that mimicked the cortex, the large surface area that controls memory and language.

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The Inquisitr web portal wrote a feature on a wide variety of efforts to create an artificial brain teeing off of this week’s publication of the cerebellum work in Cell Reports. The piece is fairly comprehensive covering computerized efforts to give robots intelligence and Europe’s Human Brain Project that is trying to map all the activity of the brain as a starting point for recapitulating it in the lab.

The experts interviewed included Robert Caplan of Tufts University in Massachusetts who is using 3-D scaffolding to build functional brain tissues that can process electrical signals. He is not planning any Frankenstein moments; he hopes to create models to improve understanding of brain diseases.

“Ideally we would like to have a laboratory brain system that recapitulates the most devastating diseases. We want to be able to take our existing toolkit of drugs and understand how they work instead of using trial and error.”

Teeth eyed as source of help for the blind. Today the European Union announced the first approval of a stem cell therapy for blindness. And already yesterday a team at the University of Pittsburg announced they had developed a new method to use stem cells to restore vision that could expand the number of patients who could benefit from stem cell therapy.

Many people have lost part or all their vision due to damage to the cornea on the surface of their eye. Even when they can gain vision back through a corneal transplant, their immune system often rejects the new tissue. So the ideal would be making new corneal tissue from the patient’s own cells. The Italian company that garnered the EU approval does this in patients by harvesting some of their own cornea-specific stem cells, called limbal stem cells. But this is only an option if only one eye is impacted by the damage.

The Pittsburgh team thinks it may have found an unlikely alternative source of limbal cells: the dental pulp taken from teeth that have be extracted. It is not as far fetched at it sounds on the surface. Teeth and the cornea both develop in the same section of the embryo, the cranial neural crest. So, they have a common lineage.

The researchers first treated the pulp cells with a solution that makes them turn into the type of cells found in the cornea. Then they created a fiber scaffold shaped like a cornea and seeded the cells on it. Many steps remain before people give up a tooth to regain their sight, but this first milestone points the way and was described in a press release from the journal Stem Cells Translational Medicine, which was picked up by the web site ClinicaSpace.

CIRM funds a project that also proposes to use the patient’s own limbal stem cells but using methods more likely to gain approval of the Food and Drug Administration than those used by the Italian company.

Stem cells and the fight against obesity. Of the two types of stem cells found in your bone marrow, one can form bone and cartilage and, all too often, fat. Preventing these stem cells from maturing into fat may be a tool in the fight against obesity according to a team at Queen Mary University of London.

The conversion of stem cells to fat seems to involve the cilia, or hair-like projections found on cells. When the cilia lengthen the stem cells progress toward becoming fat. But if the researchers genetically prevented that lengthening, they stopped the conversion to fat cells. The findings opens several different ways to think about understanding and curbing obesity says Melis Dalbay one of the authors of the study in a university press release picked up by ScienceNewsline.

“This is the first time that it has been shown that subtle changes in primary cilia structure can influence the differentiation of stem cells into fat. Since primary cilia length can be influenced by various factors including pharmaceuticals, inflammation and even mechanical forces, this study provides new insight into the regulation of fat cell formation and obesity.”

Roadmap to our epigenome reveals the genetic switches that make one adult cell type different from others

A decade ago scientists made a huge news splash when they announced the completion of the human genome project declaring it the first road map of our genes. But it did not take long to realize that the early road map was like some of the early days of GPS systems: it lacked knowledge of many on-ramps, off-ramps and one-way streets.

Today, the scientific world announced a massive fix to its genetic GPS. While all of our cells carry the same genes, their function varies wildly based one which genes are turned off, which are turned on, and even which are turned on in a hyper active way. Complex chemical and structural changes in the chromosomes that house our genes—collectively called the epigenome—determine that activity.

This video from Nature explaining the epigenome with music metaphors is linked in the last paragraph.

This video from Nature explains the epigenome with music metaphors.


A massive project, mostly funded by the National Institutes of Health through a consortium of research teams around the country, published a series of papers today in Nature. The Roadmap Epigenomic Consortium did extensive analysis of 111 epigenomes from different types of cells: normal heart tissue and immune cells, for example, as well as cells from patients with diseases such as neurons from patients with Alzheimer’s. The Scientist this morning quoted one member of the Consortium, MIT’s Manolis Kellis:

“The human epigenome is this collection of . . . chemical modifications on the DNA itself and on the packaging that holds DNA together. All our cells have a copy of the same book, but they’re all reading different chapters, bookmarking different pages, and highlighting different paragraphs and words.”

CIRM funding contributed to two of the papers authored by a team at the University of California, San Diego. One of the papers looked at how the genetic structure of stem cells changes as they mature and differentiate into specific types of adult tissue. The other looked at how structural differences determine which of the chromosomes we inherit—the one from mom or the one from dad—has a stronger influence on specific traits. The senior author on the studies, Bing Ren, noted in a university press release that these differences will be important as we think about individualizing therapies:

“Both of these studies provide important considerations for clinicians and researchers who are developing personalized medicines based on a patient’s genomic information”

The consortium’s publications today resulted from a massive data analysis. A press release from the Broad Institute in Cambridge, Massachusetts, describes the effort that required grouping two million predicted areas of change in the chromosomes into 200 sets or modules and then looking for how those modules impacted different cell types.

But if you are still having trouble understanding the concept of the epigenome, I highly recommend taking the five minutes it takes to watch this video produced by Nature. It equates the process to a symphony and what occurs when you change notes and intensity in the score.