Watch Spinal Cord Cells Take a Hike!

magic school busWhat exactly goes on inside the human body? If you asked this question to the children’s book character Ms. Frizzle, she would throw you into her Magic School Bus and take you on a wild ride “Inside the Human Body” to get you up close and personal with the different organs and structures within our bodies.

Ms. Frizzle had a wild imagination, but she was on to something with her crazy adventures. Recently, scientists took a page out of one of Ms. Frizzle children’s books and took their own wild ride to check out what’s going on with the human spinal cord.

In a paper published yesterday in Neuron, scientists from the Salk Institute in San Diego reported that they were able to watch spinal cord cells walk around the spine of mice in real-time. They used a special microscope that could track and record the movement of motor neurons, an important nerve cell that controls the movement of muscles in your body. What they found when they watched these cells was equivalent to a pot of gold at the end of the rainbow.

Check out their stunning movie here:

The scientists not only recorded the activity of these motor neurons, but they identified the other spinal cord cells that these neurons interact and make connections with. One of their most significant findings was a population of spinal cord cells that connected to a subtype of motor neurons to foster important muscle movements like walking.

Understanding how the different cells of the spinal cord work together is very important because it will allow scientists and doctors to figure out better ways to treat patients with spinal cord injuries or neurodegenerative diseases, like ALS, that affect motor neurons.

Senior author Samuel Pfaff commented in a press release on the importance of this study and how easy his team’s technology is to use:


Samuel Pfaff

Using optical methods to be able to watch neuron activity has been a dream over the past decade. Now, it’s one of those rare times when the technology is actually coming together to show you things you hadn’t been able to see before. You don’t need to do any kind of post-image processing to interpret this. These are just raw signals you can see through the eyepiece of a microscope. It’s really a jaw-dropping kind of visualization for a neuroscientist.

While this study doesn’t provide a direct avenue for therapeutic development, it does pave the way for a better understanding of the normal, healthy processes that go on in the human spine. Having more knowledge of “what is right” will help scientists to develop better strategies to fix “what is wrong” in spinal cord injuries and diseases like ALS.

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CIRM-funded clinical trial for spinal cord injury reports promising results

Today, the Menlo Park-based biotech company Asterias Biotherapeutics reported positive results from the first three patients treated in its Phase 1/2a clinical study using stem cell therapy to treat patients with spinal cord injury. This trial is funded by a CIRM Strategic Partnerships Award grant of $14.3 million.

asteriasAsterias has developed a stem cell therapy called AST-OPC1 that uses oligodendrocyte progenitor cells (OPCs), a kind of cell found in the nervous system, to treat patients that have suffered from different types of spinal cord injury. Damage to the spinal cord causes a range of paralysis based on where it occurs. People with spinal cord trauma to the mid-back often retain the use of their hands and arms but can no longer walk and may lose bladder function. Patients with spinal cord injuries in their neck  can be paralyzed completely from their neck down.

astopc1OPCs are precursors to an important cell type in the central nervous system called the oligodendrocyte. These cells are responsible for forming a conductive sheet around nerve cells that allows nerves to send electrical signals and messages safely from one nerve to another. Both OPCs and oligodendrocytes provide support and protection to nerves in the spinal cord and brain, and they can also facilitate repair of damaged nerves by secreting survival and growth factors as well as promoting the formation of new blood vessels.

In this first part of the Phase 1/2a clinical trial three patients with complete cervical (neck) spinal cord injuries were given a “low dose” of two million AST-OPC1 cells to test the safety and feasibility of their stem cell treatment. The first patient was treated at the Shepard Center in Atlanta,  and at the two month post-injection assessment, the patient experienced no side effects and an improvement from a complete to an incomplete injury on the ASIA impairment injury scale. The other two patients received injections at the Rush University Medical Center in Chicago. Both procedures were reported to have gone smoothly, and the patients are still being monitored.

Asterias plans to treat a second group of patients with higher doses of AST-OPC1 cells (10-20 millions cells). Chief Medical Officer Dr. Edward Wirth explained their strategy:

 The safety data in the first cohort now paves the way for testing the higher doses of AST-OPC1 (10-20 million cells) that we believe correspond most closely to the doses that showed the greatest efficacy in animal studies.

If both the low dose and high dose groups report no serious side effects, Asterias will turn to the Food and Drug Administration (FDA) for approval to expand the patient population of this clinical trial phase from 13 patients up to 40. Asterias hopes that adding more patients “will increase the statistical confidence of the safety and efficacy readouts, reduce the risks of the AST-OPC1 program and position the product for potential accelerated regulatory approvals.”

Spinal cord injury affects more than 12,000 people every year. It remains a major unmet medical need without any FDA-approved therapies or medical devices that improve or restore patient spinal cord function. CIRM is hopeful that Asterias will continue to see positive results with the SCiStar trial and will be able to progress its AST-OPC1 program into late-stage clinical trials and eventually into an FDA-approved stem cell therapy for spinal cord injury.

Related links

New Regenerative Liver Cells Identified

It’s common knowledge that your liver is a champion when it comes to regeneration. It’s actually one of the few internal organs in the human body that can robustly regenerate itself after injury. Other organs such as the heart and lungs do not have the same regenerative response and instead generate scar tissue to protect the injured area. Liver regeneration is very important to human health as the liver conducts many fundamental processes such as making proteins, breaking down toxic substances, and making new chemicals required to digest your food.

The human liver.

The human liver

Over the years, scientists have suggested multiple theories for why the liver has this amazing regenerative capacity. What’s known for sure is that mature hepatocytes (the main cell type in the liver) will respond to injury by dividing and proliferating to make more hepatocytes. In this way, the liver can regrow up to 70% of itself within a matter of a few weeks. Pretty amazing right?

So what is the source of these regenerative hepatocytes? It was originally thought that adult liver stem cells (called oval cells) were the source, but this theory has been disproved in the past few years. The answer to this million-dollar question, however, likely comes from a study published last week in the journal Cell.

Hybrid hepatocytes (shown in green) divide and regenerate the liver in response to injury. (Image source: Font-Burgada et al., 2015)

Hybrid hepatocytes (green) divide and regenerate the liver in response to injury. (Image source: Font-Burgada et al., 2015)

A group at UCSD led by Dr. Michael Karin reported a new population of liver cells called “hybrid hepatocytes”. These cells were discovered in an area of the healthy liver called the portal triad. Using mouse models, the CIRM-funded group found that hybrid hepatocytes respond to chemical-induced injury by massively dividing to replace damaged or lost liver tissue. When they took a closer look at these newly-identified cells, they found that hybrid hepatocytes were very similar to normal hepatocytes but differed slightly with respect to the types of liver genes that they expressed.

A common concern associated with regenerative tissue and cells is the development of cancer. Actively dividing cells in the liver can acquire genetic mutations that can cause hepatocellular carcinoma, a common form of liver cancer.

What makes this group’s discovery so exciting is that they found evidence that hybrid hepatocytes do not cause cancer in mice. They showed this by transplanting a population of hybrid hepatocytes into multiple mouse models of liver cancer. When they dissected the liver tumors from these mice, none of the transplanted hybrid cells were present. They concluded that hybrid hepatocytes are robust and efficient at regenerating the liver in response to injury, and that they are a safe and non-cancer causing source of regenerating liver cells.

Currently, liver transplantation is the only therapy for end-stage liver diseases (often caused by cirrhosis or hepatitis) and aggressive forms of liver cancer. Patients receiving liver transplants from donors have a good chance of survival, however donated livers are in short supply, and patients who actually get liver transplants have to take immunosuppressant drugs for the rest of their lives. Stem cell-derived liver tissue, either from embryonic or induced pluripotent stem cells (iPSC), has been proposed as an alternative source of transplantable liver tissue. However, safety of iPSC-derived tissue for clinical applications is still being addressed due to the potential risk of tumor formation caused by iPSCs that haven’t fully matured.

This study gives hope to the future of cell-based therapies for liver disease and avoids the current hurdles associated with iPSC-based therapy. In a press release from UCSD, Dr. Karin succinctly summarized the implications of their findings.

“Hybrid hepatocytes represent not only the most effective way to repair a diseased liver, but also the safest way to prevent fatal liver failure by cell transplantation.”

This exciting and potentially game-changing research was supported by CIRM funding. The first author, Dr. Joan Font-Burgada, was a CIRM postdoctoral scholar from 2012-2014. He reached out to CIRM regarding his publication and provided the following feedback:

CIRM Postdoctoral Fellow Jean Font-Burgada

CIRM postdoctoral scholar Joan Font-Burgada

“I’m excited to let you know that work CIRM funded through the training program will be published in Cell. I would like to express my most sincere gratitude for the opportunity I was given. I am convinced that without CIRM support, I could not have finished my project. Not only the training was excellent but the resources I was offered allowed me to work with enough independence to explore new avenues in my project that finally ended up in this publication.”


We at CIRM are always thrilled and proud to hear about these success stories. More importantly, we value feedback from our grantees on how our funding and training has supported their science and helped them achieve their goals. Our mission is to develop stem cell therapies for patients with unmet medical needs, and studies such as this one are an encouraging sign that we are making progress towards to achieving this goal.

Related links:

UCSD Press Release

CIRM Spotlight on Liver Disease Research

CIRM Spotlight on Living with Liver Disease

Building a Bridge to Therapies: Stem Cell-Derived Neurons Restore Feeling to Injured Limbs

It’s been a great week for spinal cord injury-related stem cell research – and it’s only Tuesday. In case you missed it, Asterias Biotherapeutics announced yesterday that they had treated their first clinical trial participant with an embryonic stem cell-based therapy for complete spinal cord injury. “Complete” refers to injuries that cause a total loss of feeling and movement below the site of injury.

Transplant human neurons (red) provide a bridge for the mice nerve fibers (green) to enter the spinal cord (spc). Image credit Hoeber et al. Scientific Reports

Transplanted human neurons (red) provide a bridge for the mice nerve fibers (green) to enter the spinal cord surface (spc). Image credit: Hoeber et al. Scientific Reports 5:10666

In another study also reported yesterday in Nature’s Scientific Reports, researchers at Uppsala University in Sweden made significant progress toward understanding and treating a related but different sort of injury that disrupts nerve signals coming into and out of the spinal cord. These so-called avulsion injuries are frequently seen after traffic, particularly motorcycle, accidents and lead to paralysis, loss of sensation, and chronic pain in the affected limbs. Although the ruptured nerve fibers from the limbs have the ability to extend back toward the spinal cord, inflammation from the site of injury makes the spinal cord impenetrable and blocks any restoration of normal sensory function.

To explore the potential of overcoming this spinal cord barrier, the research team transplanted human embryonic stem cell-derived neurons into mice mimicking human avulsion injury. Five months after the transplant, growth of nerve fibers into the spinal cord was seen. But these nerve fibers that had reconnected with the spinal cord were host animal cells and not the transplanted human stem cell-derived neurons. It turns out the human neuron fibers provide a physical bridge permitting the mouse nerve fibers to extend into the spinal cord. The human neurons also encourage this regrowth by releasing proteins that reduce the scar left by the injury and promote nerve fiber growth. The reconnected nerve fibers is an exciting result but did it have any impact on the animals? The answer is yes. Using standard behavior tests the team found that injured mice with the transplanted neurons had more sensitivity to touch stimulation and greater grip strength compared to untreated injured mice.

Because stem cells have the ability for unlimited growth, any future therapy based on these findings must shown that the transplant doesn’t lead to excessive cell growth. In an encouraging sign, no tumor formation or extreme growth of human neurons in the animals were observed.

Molecular Trick Diminishes Appearance of Scars, Stanford Study Finds

Every scar tells a story, but that story may soon be coming to a close, as new research from Stanford University reveals clues to why scars form—and offers clues on how scarring could become a thing of the past.

Reported last week in the journal Science, the research team pinpointed the type of skin cell responsible for scarring and, importantly, also identified a molecule that, when activated, can actually prevent the skin cells from forming a scar. As one of the study’s senior authors Michael Longaker explained in a press release, the biomedical burden of scarring is vast.

Scars, both internal and external, present a significant biomedical burden.

Scars, both internal and external, present a significant biomedical burden.

“About 80 million incisions a year in this country heal with a scar, and that’s just on the skin alone,” said Longaker, who also co-directs Stanford’s Institute for Stem Cell Biology and Regenerative Medicine. “Internal scarring is responsible for many medical conditions, including liver cirrhosis, pulmonary fibrosis, intestinal adhesions and even the damage left behind after a heart attack.”

Scars are normally formed when a type of skin cell called a fibroblast secretes a protein called collagen at the injury site. Collagen acts like a biological Band-Aid that supports and stabilizes the damaged skin.

In this study, which was funded in part by a grant from CIRM, Longaker, along with co-first authors Yuval Rinkevich and Graham Walmsley, as well as co-senior author and Institute Director Irving Weissman, focused their efforts on a type of fibroblast that appeared to play a role in the earliest stages of wound healing.

This type of fibroblast stands out because it secretes a particular protein called engrailed, which initial experiments revealed was responsible for laying down layers of collagen during healing. In laboratory experiments in mouse embryos, the researchers labeled these so-called ‘engrailed-positive fibroblast cells,’ or EPF cells, with a green fluorescent dye. This helped the team track how the cells behaved as the mouse embryo developed.

Interestingly, these cells were also engineered to self-destruct—activated with the application of diphtheria toxin—so the team could monitor what would happen in the absence of EPF cells entirely.

Their results revealed strong evidence that EPF cells were critical for scar formation. The scarring process was so tied to these EPF cells that when the team administered the toxin to shut them down, scarring reduced significantly.

Six days later the team found continued differences between mice with deactivated EPF cells, and a group of controls. Indeed, the experimental group had repaired skin that more closely resembled uninjured skin, rather than the distinctive scarring pattern that normally occurs.

Further examination of EPF cells’ precise function revealed a protein called CD26 and that blocking EPF’s production of CD26 had the same effect as shutting off EPF cells entirely. Wounds treated with a CD26 inhibitor had scars that covered only 5% of the original injury site, as opposed to 30%.

Pharmaceutical companies Merck and Novartis have already manufactured two types of CD26 inhibitor, originally developed to treat Type II diabetes, which could be modified to block CD26 production during wound healing—a prospect that the research team is examining more closely.

I Sing the Bioelectric: Long-Distance Electrical Signals Guide Cell Growth and Repair

Genes turn on, and genes turn off. Again and again, the genes that together comprise the human genome receive electrical signals that can direct when they should be active—and when they should be dormant. This intricate pattern of signals is a part of what guides an embryonic stem cell to grow and mature into any one of the many types of cells that make up the human body.

Bioelectric signals sent between cells—even cells at great distance from each other—have been found to carry important instructions relating to the growth, development and repair of organs such as the brain.

Bioelectric signals sent between cells—even cells at great distance from each other—have been found to carry important instructions relating to the growth, development and repair of organs such as the brain.

These electrical signals that guide cell growth have long been described as molecular ‘switches.’ But now, scientists at Tufts University have decoded these electrical signals—and discovered that they are far more complex than we had ever imagined.

Reporting in today’s issue of the Journal of Neuroscience, lead author Michael Levin and his Tufts research team have mapped the electrical signals transmitted between cells during development, and found that not only do these signals direct when a gene should be switched on, they also carry their own set of instructions, crucial to cellular development. Using the example of brain formation, Levin explained in today’s news release:

“We’ve found that cells communicate, even across long distances in the embryo, using bioelectrical signals, and they use this information to know where to form a brain and how big that brain should be. The signals are not just necessary for normal development; they are instructive.”

Instead of a molecular switchboard, an analogy that some have used to describe these bioelectrical signals, Levin likened the system to a computer. The signals themselves act like software programs, delivering instructions and information between cells at precisely the right time—even cells at great distance from one another.

Using tadpole embryos as a model, the team identified that the pattern of changes in voltage levels between cell membranes, called cellular resting potential, is the source of these bioelectrical signals, which are crucial to cellular development.

Specifically, the team mapped the changing voltage levels in embryonic stem cells in regards to the formation of the brain. In addition to discovering that these bioelectric signals instruct the formation of organs such as the brain, their discovery also hints at how scientists could manipulate these signals to repair tissues or organs that have been damaged—or even to grow new, healthy tissues.

“This latest research also demonstrated molecular techniques for ‘hijacking’ this bioelectric communication to force the body to make new brain tissue at other locations and to fix genetic defects that cause brain malformation,” Levin explained. “This means we may be able to induce growth of new brain tissue to address birth defects or injury, which is very exciting for regenerative medicine.”

In addition, the authors argue that modifying the bioelectrical signals to generate tissue—rather than modifying the genes themselves—may reduce the risk of adverse effects that may crop up by modifying genes directly.

While it’s early days for this work, Levin and his team foresee ways to apply this knowledge directly to medicine, for example by developing electricity-modulating drugs—which they call ‘electroceuticals’—that can repair damaged or defective tissue, and induce tissue growth.

Stay on Target: Scientists Create Chemical ‘Homing Devices’ that Guide Stem Cells to Final Destination

When injecting stem cells into a patient, how do the cells know where to go? How do they know to travel to a specific damage site, without getting distracted along the way?

Scientists are now discovering that, in some cases they do but in many cases, they don’t. So engineers have found a way to give stem cells a little help.

As reported in today’s Cell Reports, engineers at Brigham and Women’s Hospital (BWH) in Boston, along with scientists at the pharmaceutical company Sanofi, have identified a suite of chemical compounds that can help the stem cells find their way.

Researchers identified a small molecule that can be used to program stem cells (blue and green) to home in on sites of damage. [Credit: Oren Levy, Brigham and Women's Hospital]

Researchers identified a small molecule that can be used to program stem cells (blue and green) to home in on sites of damage. [Credit: Oren Levy, Brigham and Women’s Hospital]

“There are all kinds of techniques and tools that can be used to manipulate cells outside the body and get them into almost anything we want, but once we transplant cells we lose complete control over them,” said Jeff Karp, the paper’s co-senior author, in a news release, highlighting just how difficult it is to make sure the stem cells reach their destination.

So, Karp and his team—in collaboration with Sanofi—began to screen thousands of chemical compounds, known as small molecules, that they could physically attach to the stem cells prior to injection and that could guide the cells to the appropriate site of damage. Not unlike a molecular ‘GPS.’

Starting with more than 9,000 compounds, the Sanofi team narrowed down the candidates to just six. They then used a microfluidic device—a microscope slide with tiny glass channels designed to mimic human blood vessels. Stem cells pretreated with the compound Ro-31-8425 (one of the most promising of the six) stuck to the sides. An indication, says the team, Ro-31-8425 might help stem cells home in on their target.

But how would these pre-treated cells fare in animal models? To find out, Karp enlisted the help of Charles Lin, an expert in optical imaging at Massachusetts General Hospital. First, the team injected the pre-treated cells into mouse models each containing an inflamed ear. Then, using Lin’s optical imaging techniques, they tracked the cells’ journey. Much to their excitement, the cells went immediately to the site of inflammation—and then they began to repair the damage.

According to Oren Levy, the study’s co-first author, these results are especially encouraging because they point to how doctors may someday soon deliver much-needed stem cell therapies to patients:

“There’s a great need to develop strategies that improve the clinical impact of cell-based therapies. If you can create an engineering strategy that is safe, cost effective and simple to apply, that’s exactly what we need to achieve the promise of cell-based therapy.”

Scientists Send Rodents to Space; Test New Therapy to Prevent Bone Loss

In just a few months, 40 very special rodents will embark upon the journey of a lifetime.


Today UCLA scientists are announcing the start of a project that will test a new therapy that has the potential to slow, halt or even reverse bone loss due to disease or injury.

With grant funding from the Center for the Advancement of Science in Space (CASIS), a team of stem cell scientists led by UCLA professor of orthopedic surgery Chia Soo will send 40 rodents to the International Space Station (ISS). Living under microgravity conditions for two months, these rodents will begin to undergo bone loss—thus closely mimicking the conditions of bone loss, known as osteoporosis, seen in humans back on Earth.

At that point, the rodents will be injected with a molecule called NELL-1. Discovered by Soo’s UCLA colleague Kang Ting, this molecule has been shown in early tests to spur bone growth. In this new set of experiments on the ISS, the researchers hope to test the ability of NELL-1 to spur bone growth in the rodents.

The team is optimistic that NELL-1 could really be key to transforming how doctors treat bone loss. Said Ting in a news release:

“NELL-1 holds tremendous hope, not only for preventing bone loss but one day even restoring healthy bone. For patients who are bed-bound and suffering from bone loss, it could be life-changing.”

“Besides testing the limits of NELL-1’s robust bone-producing efforts, this mission will provide new insights about bone biology and could uncover important clues for curing diseases such as osteoporosis,” added Ben Wu, a UCLA bioengineer responsible for initially modifying NELL-1 to make it useful for treating bone loss.

The UCLA team will oversee ground operations while the experiments will be performed by NASA scientists on the ISS and coordinated by CASIS.

These experiments are important not only for developing new therapies to treat gradual bone loss, such as osteoporosis, which normally affects the elderly, but also those who have bone loss due to trauma or injury—including bone loss due to extended microgravity conditions, a persistent problem for astronauts living on the ISS. Said Soo:

“This research has enormous translational application for astronauts in space flight and for patients on Earth who have osteoporosis or other bone-loss problems from disease, illness or trauma.”

UC Davis Surgeons Begin Clinical Trial that Tests New Way to Deliver Stem Cells; Heal Bone Fractures

Each year, approximately 8.9 million people worldwide will suffer a bone fracture. Many of these fractures heal with the help of traditional methods, but for some, the road to recovery is far more difficult.


After exhausting traditional treatments—such as surgically implanted pins or plates, bed rest and injections to spur bone growth—these patients can undergo a special type of stem cell transplant that directs stem cells extracted from the bone marrow to the fracture site to speed healing.

This procedure has its drawbacks, however. For example, the act of extracting cells from one’s own bone marrow and then injecting them into the fracture site requires two very painful surgical procedures: one to extract the cells, and another to implant them. Recovery times for each procedure, especially in older patients, can be significant.

Enter a team of surgeons at UC Davis. Who last week announced a ‘proof-of-concept’ clinical trial to test a device that can extract and isolate stem cells far more efficiently than before—and allow surgeons to implant the cells into the fracture in just a single surgery.

As described in HealthCanal, he procedure makes use of a reamer-irrigator-aspirator system, or RIA, that normally processes wastewater during bone drilling surgery. As its name implies, this wastewater was thought to be useless. But recent research has revealed that it is chock-full of stem cells.

The problem was that the stem cells were so diluted within the wastewater that they couldn’t be used. Luckily, a device recently developed by Sacramento-based SynGen, Inc., was able to quickly and efficiently extract the cells in high-enough concentrations to then be implanted into the patient. Instead of having to undergo two procedures—the patient now only has to undergo one.

“The device’s small size and rapid capabilities allow autologous stem cell transplantation to take place during a single operation in the operation room rather than requiring two procedures separated over a period of weeks,” said UC Davis surgeon Mark Lee, who is leading the clinical trial. “This is a dramatic difference that promises to make a real impact on healing and patient recovery.”

Hear more from Lee about how stem cells can be used to heal bone fractures in our 2012 Spotlight on Disease.

Multitasking molecule repairs damaged nerve cells, scientists discover in ‘stunning’ research breakthrough

Every molecule in the body has a job to do—everything from maintaining healthy cell functions to removing dead or decaying cells requires a coordinated series of molecular switches to complete. There’s a lot we know about what these molecules do, but even more that we are still discovering.

The PSR-1 molecule, which normally clears out dead or dying nerve cells, has also been observed trying to repair them.

The PSR-1 molecule, which normally clears out dead or dying nerve cells, has also been observed trying to repair them.

And as reported in a pair of studies published this week in Nature and Nature Communications, a molecule that has long been known to clear out dying or damaged nerve cells also—amazingly—tries to heal them.

The molecule at the heart of these studies is called phophatidylserine receptor, or PSR-1 for short. PSR-1’s main job had been to target and remove cells that were dead or dying—a sort of cellular ‘cleanup crew.’

Some cells die because they’ve reached the end of their life cycle and are scheduled for destruction, a programmed cell death known as apoptosis. Other cells die because they have been damaged by disease or injury. In this study, scientists at the University of Colorado, Boulder and the University of Queensland (UQ) in Brisbane, Australia, discovered that not only does PSR-1 clear out dead cells, it tries to save the ones that haven’t quite kicked the bucket.

Specifically, the team observed PSR-1 literally reconnecting nerve fibers, known as axons, which had broken due to injury.

“I would call this an unexpected and somewhat stunning finding,” said one of the study’s lead authors Ding Xue in a news release. “This is the first time a molecule involved in apoptosis has been found to have the ability to repair severed axons, and we believe it has great therapeutic potential.”

Professor Ding Xue of the University of Colorado Boulder. [Credit: Casey A. Cass, University of Colorado]

Professor Ding Xue of the University of Colorado Boulder. [Credit: Casey A. Cass, University of Colorado]

Injuries to nerve cells that reside in the brain or spinal cord are particularly distressing because once damaged, the cells can’t be repaired. As a result, many research groups have looked to innovative ways of coaxing the cells to repair themselves. Xue and Hilliard see the potential of PSR-1 to be involved in such a strategy.

“This will open new avenues to try and exploit this knowledge in other systems closer to human physiology and hopefully move toward solving injuries,” said Hilliard.

The discovery of PSR-1’s role in axon repair is based off a key difference between cells undergoing programmed cell death and those that are dying due to injury.

During apoptosis, cells release a beacon to alert PSR-1 that they’re ready for removal. But when a nerve cell is injured, it sends out a distress signal. Explained Xue:

“The moment there is a cut to the nerve cell we see…a signal to PSR-1 molecules in the other part of the nerve that essentially says ‘I am in danger, come and save me.’”

While these experiments were performed in the model organism C. elegans (a small worm often used in this sort of research), the researchers are optimistic that a similar process is taking place in human nerve cells.

“Whether human PSR has the capacity to repair injured axons is still unknown. But I think our new research findings will spur a number of research groups to chase this question.”