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June 2020

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Nanoparticle for overcoming leukemia treatment resistance — ScienceDaily

UConn associate professor of pharmaceutics Xiuling Lu, along with professor of chemistry Rajeswari M. Kasi, was part of a team that recently published a paper in Nature Cell Biology finding a commonly used chemotherapy drug may be repurposed as a treatment for resurgent or chemotherapy-resistant leukemia.

One of the largest problems with cancer treatment is the development of resistance to anticancer therapies. Few FDA-approved products directly target leukemia stem cells, which cause treatment-resistant relapses. The only known method to combat their presence is stem cell transplantation.

Leukemia presents unique treatment challenges due to the nature of this form of cancer. The disease affects bone marrow, which produces blood cells. Leukemia is a cancer of the early blood-forming cells, or stem cells. Most often, leukemia is a cancer of the white blood cells. The first step of treatment is to use chemotherapy to kill the cancerous white blood cells, but if the leukemia stem cells in the bone marrow persist, the cancer may relapse in a therapy-resistant form.

Fifteen to 20% of child and up to two thirds of adult leukemia patients experience relapse. Adults who relapse face a less-than 30% five-year survival rate. For children the five-year survival rate after relapse is around two thirds. When relapse occurs, chemotherapy does not improve the prognosis for these patients. There is a critical need for scientists to develop a therapy that can more effectively target chemotherapy-resistant cells.

There are two cellular pathways, Wnt- β-catenin and PI3K-Akt, which play a key role in stem cell regulation and tumor regenesis. Cooperative activation of the Wnt- β-catenin and PI3K-Akt pathways drives self-renewal of cells that results in leukemic transformation, giving rise to cancer relapse. Previous studies have worked on targeting elements of these pathways individually, which has had limited success and often results in the growth of chemo-resistant clones.

The researchers screened hundreds of drugs to find one that may inhibit this interaction. They identified a commonly used chemotherapy drug, doxorubicin as the most viable target. While this drug is highly toxic and usually used with caution in clinical settings, the team found when used in multiple, low doses, it disrupts the Wnt- β-catenin and PI3K-Akt pathways’ interaction, while potentially reducing toxicity.

Lu’s lab contributed a nanoparticle which allowed the drug to be injected safely and released sustainably over time, a key to the experiment’s success. The nanoparticle encasing doxorubicin enables slow release of the drug to the bone marrow to reduce the Akt-activated Wnt– β-catenin levels in chemo-resistant leukemic stem cells and reduce the tumorigenic activity. In low doses, doxorubicin stimulated the immune system while typical clinical doses are immunosuppressive, inhibiting healthy immune cells.

Lu is the CEO of Nami Therapeutics, a startup which designs nanoparticles for drug delivery in a variety of clinical contexts including cancer treatment and vaccine delivery.

Because of its rate of drug release, Lu’s patented nanoparticle was more effective than both a solution of the pure drug and a liposomal doxorubicin, the only commercially available version of a nanoparticle carrying doxorubicin.

“It’s exciting that the whole research team identified this new mechanism to effectively inhibit leukemia stem cells,” Lu says. “We are happy to see that our proprietary nanoparticle delivery system has such potential to help patients.”

By using low, but more sustained, doses of this drug, leukemia-initiating activity of cancerous stem cells was effectively inhibited.

The researchers demonstrated clinical relevance by transplanting patient leukemic cells into mice and observing that low-dose doxorubicin’s ability to disrupt these cells. Patient sample transplants with therapy-resistant leukemia stem cells rapidly developed leukemia. But the low-dose doxorubicin nanoparticle treatment improved survival by reducing the presence of leukemia stem cells.

Lu says the next steps for this research is to further validate the now-patented method and nanoparticle and eventually bring it into clinical usage. Lu and her collaborator, Rajeswari Kasi, also have two pending patents on copolymer-nanoparticles for drug delivery and methods for treating chemo-resistant cancer-initiating cells.

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Cord blood for stem cell transplant may outperform matched sibling donor — ScienceDaily

When a cancer patient needs a bone marrow transplant, there are four common donor sources: A matched related donor (sibling), a matched unrelated donor (from a donor database), a half-matched donor, or umbilical cord blood. Of course, there are plusses and minuses to each approach, but consensus has generally ranked a matched sibling first, followed by a matched unrelated donor, with cord blood and half-matched donors reserved for patients without either of the first two options.

Now a University of Colorado Cancer Center study based on a decade of research and treatment may reshuffle this list. In fact, the comparison of 190 patients receiving cord-blood transplants with 123 patients receiving transplants from the “gold standard” of matched sibling donors showed no difference in survival outcomes between these two approaches, with significantly fewer complications due to chronic graft-versus-host disease in patients receiving transplants from cord blood.

“Our cord blood patients were doing as well as patients receiving transplants from matched siblings, and in selected populations cord blood patients were doing even better. Our program at CU Cancer Center is somewhat unique in its emphasis on cord blood as a donor source for stem cell transplants and this study is an affirmation of why we do what we do here,” says Jonathan Gutman, MD, CU Cancer Center investigator and director of the allogeneic stem cell transplantation program at UCHealth University of Colorado Hospital.

In addition to showing a decrease in the chance of graft-versus-host disease, which develops when a transplanted blood system attacks a patient’s tissues, the study shows a slightly lower rate of relapse in these patients undergoing transplant with cord blood.

“Especially with younger, fitter patients who we can hit harder in the transplant process, we have strong hints here that cord blood may be actively better in terms of reducing both graft-versus-host disease and relapse,” Gutman says.

Umbilical cord blood, which is banked for public use at designated centers around the world, is rich in stem cells, which can repopulate a patient’s blood system. Because these umbilical cord stem cells are more “basic” than adult blood cells, they require a lower degree of match than blood cells from an adult donor. However, one challenge has been obtaining enough of these cells to perform a successful transplant.

“It turns out that for adults, it’s very hard to find a single cord blood unit that meets the parameters we know need to be met in terms of size. To overcome this barrier, we often use two units from different sources,” Gutmans says. Also, research at CU Cancer Center and elsewhere is developing techniques to expand small samples of banked cord blood to the volume needed for transplant.

“We think there are important advantages of cord blood, especially with respect to graft-versus-host disease,” Gutman says. “Previously, we’ve taken a position recommending cord blood over matched unrelated donors, and now we show that cord blood may even out-compete the gold standard of matched sibling donors.”

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Materials provided by University of Colorado Anschutz Medical Campus. Original written by Garth Sundem. Note: Content may be edited for style and length.

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Texas A&M researchers say these grafts could be used to promote swift and precise bone healing — ScienceDaily

Although most broken bones can be mended with a firm cast and a generous measure of tender loving care, more complicated fractures require treatments like bone grafting. Researchers at Texas A&M University have now created superior bone grafts using primitive stem cells. They found that these cells help create very fertile scaffolds needed for bone to regenerate at the site of repair.

The researchers said these grafts could be used to promote swift and precise bone healing so that patients maximally benefit from the surgical intervention.

“There are several problems that can occur with orthopedic implants, like inflammation and pain. Also, they can loosen, requiring revision surgeries that are often more complicated than the original surgery to put in the implant,” Dr. Roland Kaunas, associate professor in the Department of Biomedical Engineering and a corresponding author on the study. “So, by speeding up the bone healing process, our material can potentially reduce the number of these revision surgeries.”

The researchers have published their findings in the June issue of the journal Nature Communications.

Each year, around 600,000 people in the United States experience delayed or incomplete bone healing. For some of these cases, physicians turn to surgical procedures that involve transplanting bone tissue to the repair site. These bone grafts have generally come from two sources: the patient’s own bone from another location on the body called autografts, or highly-processed human cadaver bones.

However, both types of bone grafts have their share of drawbacks. For example, autografts require additional surgery for bone tissue extraction, increasing the recovery time for patients and sometimes, chronic pain. On the other hand, grafts derived from cadaver bone preclude the need for two surgeries, but these transplants tend to be devoid of many of the biomolecules that promote bone repair.

“Grafts from cadaver bone have some of the physical properties of bone, and even a little bit of the biological essence but they are very depleted in terms of their functionality,” said Dr. Carl Gregory, associate professor at the Texas A&M Health Science Center, also a corresponding author on the study. “What we wanted to do was engineer a bone graft where we could experimentally crank up the gears, so to speak, and make it more biologically active.”

Previous studies have shown that stem cells, particularly a type called mesenchymal stem cells, can be used to produce bone grafts that are biologically active. In particular, these cells convert to bone cells that produce the materials required to make a scaffolding, or the extracellular matrix, that bones need for their growth and survival.

However, these stem cells are usually extracted from the marrow of an adult bone and are, as a result, older. Their age affects the cells’ ability to divide and produce more of the precious extracellular matrix, Kaunas said.

To circumvent this problem, the researchers turned to the cellular ancestors of mesenchymal stem cells, called pluripotent stem cells. Unlike adult mesenchymal cells that have a relatively short lifetime, they noted that these primitive cells can keep proliferating, thereby creating an unlimited supply of mesenchymal stem cells needed to make the extracellular matrix for bone grafts. They added that pluripotent cells can be made by genetically reprogramming donated adult cells.

When the researchers experimentally induced the pluripotent stem cells to make brand new mesenchymal stem cells, they were able to generate an extracellular matrix that was far more biologically active compared to that generated by mesenchymal cells obtained from adult bone.

“Our materials were not just enriched in the biological molecules that are required to make the chunky part of bone tissue but also growth factors that drive blood vessel formation,” said Gregory.

To test the efficacy of their scaffolding material as a bone graft, they then carefully extracted and purified the enriched extracellular matrix and then implanted it at a site of bone defects. Upon examining the status of bone repair in a few weeks, they found that their pluripotent stem-cell-derived matrix was five to sixfold more effective than the best FDA-approved graft stimulator.

“Bone repair assays using the gold standard of grafts, like those administered with the powerful bone growth stimulator called bone morphogenic protein-2, can take about eight weeks, but we were getting complete healing in four weeks,” said Gregory. “So, under these conditions, our material surpassed the efficacy of bone morphogenic protein-2 by a longshot, indicating that it is a vast improvement of current bone repair technologies.”

The researchers also said that from a clinical standpoint, the grafts can be incorporated into numerous engineered implants, such as 3D-printed implants or metal screws, so that these parts integrate better with the surrounding bone. They also noted that the bone grafts will also be easier to produce and hence are advantageous from a manufacturing standpoint.

“Our material is very promising because the pluripotent stem cells can ideally generate many batches of the extracellular matrix from just a single donor which will greatly simplify the large-scale manufacturing of these bone grafts,” said Kaunas.

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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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