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Researchers uncover drivers of healthy gut maintenance — ScienceDaily

Researchers at the Francis Crick Institute have found two genes that regulate the differentiation of stem cells in the small intestine, offering valuable insight into how the body develops and maintains a healthy gut.

Cells in the lining of the small intestine are replaced around every five days, the quickest rate for any organ in the body. This fast replacement helps the lining cope with the damage it suffers as a result of breaking down food and absorbing nutrients.

This process, which is important for the healthy functioning of the small intestine, is supported by the stem cells in a part of the small intestine called the crypt.

In their study, published in Gastroenterology, the researchers found two genes, MTG8 and MTG16, which are highly expressed in cells that have just left the stem cell zone. These genes ‘switch off’ signals that keep these cells in a multipotent or ‘immature’ state, leading them to start to differentiate.

When the team analysed intestinal tissue and small intestine organoids grown from mice lacking these genes, they found there were many more stem cells, indicating that the process of differentiation was impeded.

Anna Baulies, lead author and postdoctoral training fellow in the Stem Cell and Cancer Biology lab at the Crick says: “These genes maintain the flow of cells which are needed for the healthy functioning of the small intestine, starting the stem cells on the road to become enterocyte cells which are needed to absorb nutrients.”

Importantly, by working with human small intestine organoids, the researchers also found that while the stem cells are still in the crypt, these genes are repressed by a key developmental pathway, Notch signalling. This ensures the stem cells do not differentiate too early.

Vivian Li, senior author and group leader of the Stem Cell and Cancer Biology lab at the Crick says, “Understanding the role these genes play in healthy tissue will also help us to understand how the intestine regularly regenerates and also if these genes are a helpful or harmful force in the presence of disease.”

“For example, loss of these genes may increase the number of stem cells and contribute to colorectal cancer progression. Further study on the underlying mechanism might be helpful to limit the number of stem cells in the cancer.”

The signal that these genes repress, Wnt signalling, also keeps stem cells in a multipotent state in many other tissues, including the skin, stomach, liver and brain. These findings could therefore help other research into stem cell differentiation outside of the small intestine.

The researchers will continue this work, looking to understand more about the mechanism these two genes use to regulate stem cell differentiation and regeneration.

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Materials provided by The Francis Crick Institute. Note: Content may be edited for style and length.

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Researchers model human stem cells to identify degeneration in glaucoma — ScienceDaily

More than 3 million Americans have glaucoma, a serious eye condition causing vision loss. Using human stem cell models, researchers at Indiana University School of Medicine found they could analyze deficits within cells damaged by glaucoma, with the potential to use this information to develop new strategies to slow the disease process.

The study, published June 11 in Stem Cell Reports, focused on targeting genetic mutations within retinal ganglion cells, which serve as the connection between the eye and the brain. Researchers found that when differentiating pluripotent human stem cells into retinal ganglion cells, they were able to identify characteristics associated with neurodegeneration in glaucoma.

“Once you’ve identified a target like this — what’s going wrong in the cells — this opens up a number of possibilities for the eventual development of therapeutic approaches, especially pharmacology approaches to slow down and reverse these degenerative phenotypes,” said Jason Meyer, PhD, associate professor of medical and molecular genetics at IU School of Medicine.

The team of researchers was led by Meyer, along with the co-first authors of the publication, Kirstin VanderWall and Kang-Chieh Huang, graduate students from the School of Science at IUPUI in Meyer’s lab, which is located within Stark Neurosciences Research Institute. Meyer’s lab had previously been located within the School of Science.

When retinal ganglion cells degenerate through glaucoma, it leads to the loss of vision and eventual blindness. Researchers in this study derived pluripotent stem cells from a patient that had a genetic form of glaucoma, Meyer said. They then differentiated the stem cells into retinal ganglion cells to search for neurodegeneration deficits.

“One of the powerful things about (stem cell research) is when you get the cells from a patient that has a genetic basis for a disease, all of the blueprints are there in the cell’s DNA to develop features of the disease,” Meyer said.

They also used gene editing technology — CRISPR-Cas9 — to introduce a genetic mutation commonly associated with glaucoma into existing lines of the stem cells for disease modeling, as well as to correct the gene defect in patient-derived cells.

“CRISPR/Cas9 gene editing approaches not only allowed us to study the disease, but using this approach we were also able to show how correcting the gene mutation reversed the disease, demonstrating the potential for gene therapy approaches as well,” Huang said.

Meyer said the team discovered dysfunction in the process of autophagy, the body’s way of removing damaged cells to regenerate healthy cells.

“We found that in the glaucoma patient cells, there are some deficits in this autophagy process, so you had too much cellular junk that was being built up,” Meyer said, adding that those deficits correlated with the degeneration of the cells, which would shrivel up and eventually die off.

Using a pharmaceutical compound called rapamycin — which is known to boost the process of autophagy — Meyer said they found that many of the neurodegenerative characteristics they had previously identified slowed down and the cells seemed to recover and appear more normal.

Meyer said human stem cells are instrumental in studying human disease, especially neurodegeneration. Past studies on retinal ganglion cells and glaucoma as a degenerative disease using animal models suggest differences in how cells respond between species.

“Since they are human cells, it gives somewhat of a more representative model for us to test pharmacological compounds,” VanderWall added, “and it gives us a better idea of how it could potentially be toxic or nontoxic to human cells compared to testing compounds in animals.”

Meyer said having identified a target within the cells — the process of autophagy — the lab’s ongoing work will focus on analyzing ways to use different types of pharmaceutical compounds for treatment of glaucoma. As is the case for many neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases, there are very few treatments, if any, and no cures.

“There is a dire need to try and identify new approaches to treat these diseases,” Meyer said. Grant support for this research was provided by the National Eye Institute, the Indiana Department of Health Spinal Cord and Brain Injury Research Fund and the Indiana Clinical and Translational Sciences Institute.

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Researchers use stem cells from adults with depression to test treatments — ScienceDaily

A study published in Molecular Psychiatry shows that patient-derived adult stem cells can be used to model major depressive disorder and test how a patient may respond to medication.

Using stem cells from adults with a clinical diagnosis of depression, the University of Illinois at Chicago researchers who conducted the study also found that fish oil, when tested in the model, created an antidepressant response.

UIC’s Mark Rasenick, principal investigator of the study, says that the research provides a number of novel findings that can help scientists better understand how the brain works and why some people respond to drug treatment for depression, while others experience limited benefits from antidepressant medication.

“It was also exciting to find scientific evidence that fish oil — an easy-to-get, natural product — may be an effective treatment for depression,” said Rasenick, UIC distinguished professor of physiology and biophysics and psychiatry at the College of Medicine.

Major depressive disorder, or depression, is the most common psychiatric disorder. Around one in six individuals will experience at least one depressive episode in their lifetime. However, antidepressant treatment fails in about one-third of patients.

In the study, the UIC researchers used skin cells from adults with depression that were converted into stem cells at Massachusetts General Hospital and then directed those stem cells to develop into nerve cells. The skin biopsies were taken from two types of patients: people who previously responded to antidepressant treatment and people who have previously been resistant to antidepressants.

When fish oil was tested, the models from treatment-sensitive and treatment-resistant patients both responded.

Rasenick says the response was similar to that seen from prescription antidepressants, but it was produced through a different mechanism.

“We saw that fish oil was acting, in part, on glial cells, not neurons,” said Rasenick, who is also a research career scientist at Jesse Brown VA Medical Center and president and chief scientific officer at Pax Neuroscience, a UIC startup company. “For many years, scientists have paid scant attention to glia — a type of brain cell that surrounds neurons — but there is increasing evidence that glia may play a role in depression. Our study suggests that glia may also be important for antidepressant action.

“Our study also showed that a stem cell model can be used to study response to treatment and that fish oil as a treatment, or companion to treatment, for depression warrants further investigation,” Rasenick said.

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Materials provided by University of Illinois at Chicago. Note: Content may be edited for style and length.

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Putting ‘super’ in natural killer cells — ScienceDaily

Using induced pluripotent stem cells (iPSCs) and deleting a key gene, researchers at University of California San Diego School of Medicine have created natural killer cells — a type of immune cell — with measurably stronger activity against a form of leukemia, both in vivo and in vitro.

The findings are published in the June 11, 2020 online issue of Cell Stem Cell.

Natural killer (NK) cells are lymphocytes in the same family as T and B cells, and are part of the innate immune system. They circulate throughout the body and are among the first to respond to the presence of foreign cells or invaders, most notably viruses and early signs of cancer.

As such, they hold great promise as the basis for anticancer therapies, able to identify and target malignant cells, but their efficacy has proven limited.

In the new study, a research team led by senior author Dan Kaufman, MD, PhD, professor of medicine in the Division of Regenerative Medicine, director of cell therapy at UC San Diego School of Medicine and a faculty member of both the Sanford Consortium for Regenerative Medicine and the Sanford Stem Cell Clinical Center at UC San Diego Health, advanced their potential in two ways.

First, they created NK cells from IPSCs, which are derived from skin or blood cells that have been reprogrammed back to an embryonic-like pluripotent state and then directed to become NK cells. This strategy produces a standardized cell population, rather than needing to isolate cells on a patient-specific basis

Second, the researchers deleted a gene called CISH in the stem cell-derived NK cells. The CISH gene regulates expression of a protein that suppresses cytokine signaling. Cytokines are molecules that signal other immune system cells, such as macrophages, lymphocytes and fibroblasts to sites of infection, inflammation and trauma.

“Deletion of CISH in NK cells removes an internal ‘checkpoint’ that is normally activated or expressed when NK cells are stimulated by cytokines, such as IL15,” said Kaufman. “We found that CISH-deleted iPSC-derived NK cells were able to effectively cure mice that harbor human leukemia cells, whereas mice treated with the unmodified NK cells died from the leukemia.”

“These studies demonstrate that we can now edit iPSC-derived NK cells to remove an inhibitory gene inside the cell to improve activation of NK cells. We demonstrate that the CISH deletion improves NK cell function in at least two different ways. First, it removes a brake on IL15 signaling, with improves NK cell activation and function, even at low IL15 concentrations. Second, it leads to metabolic reprogramming of the NK cells. They become more efficient at energy utilization, which improves their function in vivo.”

Kaufman said he and colleagues are now working to translate the findings into a clinical therapy.

“As iPSC-derived NK cells are now in clinical trials to treat both hematologic (blood) malignancies and solid tumors, we expect that CISH-deleted iPSC-NK cells can provide an even more effective treatment.

“Importantly, iPSCs provide a stable platform for gene modification and since NK cells can be used as allogeneic cells that do not need to be matched to individual patients, we can create a line of appropriately modified iPSC-derived NK cells suitable for treating hundreds or thousands of patients as a standardized, ‘off-the-shelf’ therapy.”

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Materials provided by University of California – San Diego. Original written by Scott LaFee. Note: Content may be edited for style and length.

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Potential treatment for Rett Syndrome — ScienceDaily

An experimental cancer drug can extend the life of mice with Rett Syndrome, a devastating genetic disorder that afflicts about one of every 10,000 to 15,000 girls within 6 to 18 months after birth, Yale researchers report June 10 in the journal Molecular Cell.

In addition, the drug JQ1 also restores the cellular function of neurons in human models of the disease. Rett Syndrome causes severe deficits in language, learning and other brain functions and eventually leads to death, often during teenage years.

The Yale team — led by senior author In-Hyun Park, associate professor of genetics, and a researcher at Yale’s Child Study Center and Stem Cell Center — wanted to know how a mutation in gene MECP-2 causes the severe disruption to neuronal functions in the cortex of Rett Syndrome patients.

They created a human brain organoid containing this mutation from embryonic stem cells and found severe abnormalities in multiple brain cells. A type of brain cell called interneurons, which regulate the brain’s excitatory neurons, was particularly impacted by the mutation.

The lab then screened a variety of compounds and found that one drug, JQ1, corrected abnormalities found in interneurons of the Rett Syndrome model. The drug has been investigated in several experimental trials as a potential cancer treatment. They then tested the drug in mice models of Rett Syndrome and found that the treated mice lived about twice as long as those not receiving the drug.

Park said the research paves the way for additional research on potential new therapies for Rett Syndrome, for which there are currently no effective treatments.

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Materials provided by Yale University. Original written by Bill Hathaway. Note: Content may be edited for style and length.

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Injected stem cells rebuild the skin’s normal elastin network, study reports — ScienceDaily

For a while now, some plastic surgeons have been using stem cells to treat aging, sun-damaged skin. But while they’ve been getting good results, it’s been unclear exactly how these treatments — using adult stem cells harvested from the patient’s own body — work to rejuvenate “photoaged” facial skin.

A new microscopic-level study provides the answer: within a few weeks, stem cell treatment eliminates the sun-damaged elastin network and replacing them with normal, undamaged tissues and structures — even in the deeper layers of skin.

Injection of the patient’s own mesenchymal stem cells (MSCs) is “appropriate, competent and sufficient to elicit the full structural regeneration of the sun-aged skin,” according to the report by Dr. Luis Charles-de-Sá, MD, of Universidade Federal do Rio de Janeiro, Brazil, Natale Gontijo-Amorim, MD and Gino Rigotti, MD of Verone-Italy University and colleagues. Their study appears in the June issue of Plastic and Reconstructive Surgery®, the official medical journal of the American Society of Plastic Surgeons (ASPS).

The researchers assessed the cellular- and molecular-level effects of MSC treatment on sun-damaged (photoaged) facial skin. All 20 patients in the study, average age 56 years, were scheduled for facelift surgery. The patients lived in northeast Brazil, a region where intense sun exposure is expected.

For each patient, a small sample of fat cells from the abdomen was processed to create patient-specific MSCs. The cultured stem cells were injected under the skin of the face, in front of the ear. When the patients underwent facelift surgery three to four months later, skin samples from the stem cell-treated area were compared to untreated areas.

Histologic and structural under the microscope analysis demonstrated that MSC treatment led to improvement in overall skin structure. Treated areas showed “partial or extensive reversal” of sun-related damage to the skin’s stretchy elastin network — the main skin structure affected by photoaging. In the layer immediately beneath the skin surface, the stem cell-treated areas showed regeneration of a new, fully organized network of fiber bundles and dermal ECM remodeling changes.

In the deeper skin layer, “tangled, degraded, and dysfunctional” deposits of sun-damaged elastin were replaced by a normal elastin fiber network. These changes were accompanied by molecular markers of processes involved in absorbing the abnormal elastin and development of new elastin.

The findings suggested that stem cells triggered each of the many cellular- and molecular-level pathways involved in skin repair and regeneration. Use of the patient’s own fat-derived MSCs “may be a relevant proposal for the anti-ageing action in regeneration of photodamaged human skin,” Dr. Charles-de-Sá and colleagues write.

“The researchers conclude that stem-cells can lead to regeneration of sun-aged skin,” according to a video commentary by Plastic and Reconstructive Surgery Editor-in-Chief Rod J. Rohrich, MD. In his video, Dr. Rohrich walks viewers through the dramatic changes in the microscopic appearance of skin samples obtained before and after MSC treatment.

“The re-building of structures below the surface translates to true improvements to the strength and appearance of the facial dermis,” Dr. Rohrich adds. He emphasizes that patients interested in stem-cell treatment for aging, sun-damaged skin should discuss their options with a Board-certified plastic surgeon.

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Materials provided by Wolters Kluwer Health. Note: Content may be edited for style and length.

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Model of the early embryonic brain — ScienceDaily

We know a lot about the human brain, but very little about how it is formed. In particular, the stages from the second to the seventh week of embryonic development have so far been virtually unknown territory to brain researchers.

To learn more about this particular period, researchers from the Department of Neuroscience and the Novo Nordisk Foundation Center for Stem Cell Biology at the Faculty of Health and Medical Sciences have now developed a model that mimics these early stages of the human brain in the laboratory.

The model is based on embryonic stem cells grown in a microfluidic system developed in collaboration with bioengineers from Lund University in Sweden.

‘We know that in the early embryonic stage the brain is exposed to various concentrations of growth factors which induces the formation of different brain regions. By using microfluidic methods, we can — under extremely controlled conditions — recreate the environment found in the early embryo, explains the first author on the study, Assistant Professor Pedro Rifes.

‘When we expose stem cells to the controlled environment, we can create a tissue that resembles an embryonic brain at a very early stage, about 4-5 weeks after fertilisation of the egg — a stage that we have so far not been able to study’.

The Developmental Tree of the Human Brain

The researchers will use the new model to make a map of the development of the brain cells — a kind of ‘Developmental tree’ of the brain, thereby learning new things about how the enormous complexity of different nerve cells in the human brain is formed during the early embryonic stages.´

‘For the first time, we have access to a tissue that resembles the early embryonic brain, and this allows us togo in and analyse what happens to each individual cell at each stage of development’, says the principal scientist behind the study, Associate Professor Agnete Kirkeby.

The idea is that brain researchers around the world will be able to use this ‘Developmental tree’ of the brain as a guide to produce different types of nerve cells for stem cell therapy. By studying the natural development of the nerve cells, the researchers will be able to speed up the creation of recipes for producing specific nerve cells in the laboratory.

A Recipe for Stem Cell Treatment

Agnete Kirkeby is well aware of the importance of a faster path to stem cell treatments. Together with colleagues from Lund and Cambridge, she has for several years worked on developing a stem cell therapy for Parkinson’s disease. This project required Kirkeby and her colleagues to produce a very specific type of nerve cells, the dopaminergic nerve cells, which are the cells that are lost in Parkinson’s Disease.

‘We have come a long way in the project and will soon be able to test the stem cell treatment in humans for the first time. But it took us more than 10 years to get this far because we depended on a trial-and-error methodology to develop the right nerve cells from the stem cells’.

With knowledge from the new model, the researchers expect to be able to considerably shorten this process in the future.

‘If we understand exactly how the brain develops in the early stages, we will become better at guiding the stem cells in the right direction when producing human nerve cells in the lab. This will allow us to more quickly and efficiently develop cell treatments for neurological diseases such as epilepsy, Parkinson’s Disease and certain types of dementia’, says Agnete Kirkeby.

New Options for testing Environmental Toxins

In addition to increasing our knowledge on brain development and easing the path to future stem cell treatments, Agnete Kirkeby believes that the embryonic brain model may serve other useful purposes as well.

‘The model may be used to investigate how brain cells in the early embryonic stages react to certain chemicals surrounding us in our daily lives — these might be substances in our environment, in consumer products or in the medications that some pregnant women may require. So far, we have not had a good model to test precisely this’.

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A new algorithm combines gradient methods with fast Fourier transforms to quantify the organization of cardiac myofibrils — ScienceDaily

Heart disease is the leading cause of death in the United States and other industrialized nations, and many patients face limited treatment options. Fortunately, stem cell biology has enabled researchers to produce large numbers of cardiomyocytes, the cells that make up the heart or cardiac muscle and have the potential to be used in advanced drug screens and cell-based therapies.

One of the pitfalls of these stem cell-generated cardiomyocytes is that they do not represent adult human cardiomyocytes but remain immature without further intervention. Additionally, current image analysis techniques do not allow researchers to analyze heterogeneous, multidirectional, striated myofibrils typical of immature cells to determine when new interventions are coaxing the cells to organize.

In the Journal of Applied Physics, from AIP Publishing, researchers showcase an algorithm that combines gradient methods with fast Fourier transforms, the scanning gradient Fourier transform or SGFT technique, to quantify myofibril structures in heart cells with considerable accuracy. Myofibrils are the elongated contractile unit of a muscle cell.

“If you look at adult human cardiac tissue, everything is not in perfect alignment. Everything is not stacked nicely and neatly like a bookshelf,” said Wendy Crone, an author of the paper. “The structures are more complicated. We wanted to be able to quantify the organization.”

This level of analysis, combined with new emerging studies of the effects of cell mutation, has the potential to produce new insights regarding the mechanisms underlying the generation of myofibrils and various cardiomyopathies, which make it harder for the heart muscle to pump blood to the rest of the body.

“There is myofibril disarray in certain diseases of the heart,” said Crone. “With our technique, we can quantify the disarray, which provides a better understanding of the severity of disease in heart cells.”

The heterogeneous, striated patterning that this new method can detect and quantify occurs in countless other instances in biology and elsewhere. For instance, the SGFT technique clearly detects the distribution of collagen organization and orientation in breast tissue biopsies, which is significant since breast tissue with cancer has more organized collagen structures. As prior studies have shown, the morphology of collagen fibers in breast cancer tissue is a strong prognostic indicator of the malignancy of the tumor.

The SGFT technique could also potentially be used to quantify striated patterns in early stage neurons derived from stems cells.

“Our code can quantify the organization of neural rosettes, too,” said Crone.

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Materials provided by American Institute of Physics. Note: Content may be edited for style and length.

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New research into stem cell mutations could improve regenerative medicine — ScienceDaily

Research from the University of Sheffield has given new insight into the cause of mutations in pluripotent stem cells and potential ways of stopping these mutations from occurring.

The findings, published in Stem Cell Reports, show that pluripotent stem cells are particularly susceptible to DNA damage and mutations compared to other cells, and this could cause genetic mutations.

Pluripotent stem cells are able to develop into any cell type in the body, and there is considerable interest in using them to produce cells to replace diseased or damaged tissues in applications referred to as regenerative medicine.

One concern for the safety of this is that these cells often acquire recurrent mutations which might lead to safety issues if used in patients.

The researchers have found that these mutations are more likely to occur in a certain point during their cell cycle and have suggested ways of growing the cells to dramatically reduce the susceptibility to DNA damage and potentially the mutations that arise.

Peter Andrews, Professor of Biomedical Science at the University of Sheffield, said: “Clinical trials of regenerative medicine using cells derived from pluripotent stem cells are now beginning around the world, but there are concerns that mutations in the pluripotent stem cells may risk patient safety. Our results may allow us to significantly reduce that risk.

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Materials provided by University of Sheffield. Note: Content may be edited for style and length.

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Findings could lead to better methods for creating muscle cells from stem cells — ScienceDaily

An interdisciplinary team of researchers at the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at UCLA has developed a first-of-its-kind roadmap of how human skeletal muscle develops, including the formation of muscle stem cells.

The study, published in the peer-reviewed journal Cell Stem Cell, identified various cell types present in skeletal muscle tissues, from early embryonic development all the way to adulthood. Focusing on muscle progenitor cells, which contribute to muscle formation before birth, and muscle stem cells, which contribute to muscle formation after birth and to regeneration from injury throughout life, the group mapped out how the cells’ gene networks — which genes are active and inactive — change as the cells mature.

The roadmap is critical for researchers who aim to develop muscle stem cells in the lab that can be used in regenerative cell therapies for devastating muscle diseases, including muscular dystrophies, and sarcopenia, the age-related loss of muscle mass and strength.

“Muscle loss due to aging or disease is often the result of dysfunctional muscle stem cells,” said April Pyle, senior author of the paper and a member of the Broad Stem Cell Research Center. “This map identifies the precise gene networks present in muscle progenitor and stem cells across development, which is essential to developing methods to generate these cells in a dish to treat muscle disorders.”

Researchers in Pyle’s lab and others around the world already have the capacity to generate skeletal muscle cells from human pluripotent stem cells — cells that have the ability to self-renew and to develop into any cell type in the body. However, until now, they had no way of determining where these cells fall on the continuum of human development.

“We knew that the muscle cells we were making in the lab were not as functional as the fully matured muscle stem cells found in humans,” said Haibin Xi, first author of the new paper and an assistant project scientist in Pyle’s lab. “So we set out to generate this map as a reference that our lab and others can use to compare the genetic signatures of the cells we are creating to those of real human skeletal muscle tissue.”

To create this resource, the group gathered highly specific data about two different groups of skeletal muscle cells: those from the human body, ranging from the fifth week of embryonic development to middle age, and those derived from human pluripotent stem cells the researchers generated in the lab. They then compared the genetic signatures of cells from both sources.

The group obtained 21 samples of human skeletal muscle tissue from their UCLA collaborators and from colleagues at the University of Southern California and the University of Tübingen in Germany. For the pluripotent stem cell-derived muscle cells, the group evaluated cells created using their own unique method and the methods of several other groups.

The Pyle lab collaborated with the lab of Kathrin Plath, a UCLA professor of biological chemistry and member of the Broad Stem Cell Research Center, to conduct high-throughput droplet-based single-cell RNA sequencing of all of the samples. This technology enables researchers to identify the gene networks present in a single cell and can process thousands of cells at the same time. Leveraging the power of this technology and the Plath lab’s bioinformatics expertise, the group identified the genetic signatures of various cell types from human tissues and pluripotent stem cells.

They next developed computational methods to focus on muscle progenitor and stem cells and mapped out their gene networks associated with every developmental stage. This enabled the group to match the genetic signatures found in the pluripotent stem cell-derived muscle cells with their corresponding locations on the map of human muscle development.

The group found that pluripotent stem cell-derived muscle cells produced by all the methods they tried resembled muscle progenitor cells at an early developmental state and did not align to adult muscle stem cells.

In addition to pinning down the true maturity of the lab-produced cells, this analysis also provided details about the other cell types present in skeletal muscle tissue across development and in populations derived from human pluripotent stem cells. These cells could play an essential role in muscle cell maturation and could be critical to improving methods to generate and support muscle stem cells in a dish.

“We found that some methods to generate muscle cells in a dish also produce unique cell types that likely support the muscle cells,” said Pyle, who is also a member of the UCLA Jonsson Comprehensive Cancer Center. “And so now our questions are, what are these cells doing? Could they be the key to producing and supporting mature and functional muscle stem cells in a dish?”

Moving forward, Pyle and her colleagues will focus on harnessing this new resource to develop better methods for generating muscle stem cells from human pluripotent stem cells in the lab. She hopes that by focusing on the stem cell-associated gene expression networks and supportive cell types they identified, they can produce high-powered muscle stem cells that can be useful for future regenerative therapies.

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