Category Archives: Stem Cell Videos

ScienceDaily (July 18, 2012) To build a tooth, a detailed recipe to instruct cells to differentiate towards proper lineages and form dental cells is needed. Researchers in the group of Professor Irma Thesleff at the Institute of Biotechnology in Helsinki, Finland have now found a marker for dental stem cells. They showed that the transcription factor Sox2 is specifically expressed in stem cells of the mouse front tooth.

Despite the development of new bioengineering protocols, building a tooth from stem cells remains a distant goal. Demand for it exists as loss of teeth affects oral health, quality of life, as well as ones appearance. To build a tooth, a detailed recipe to instruct cells to differentiate towards proper lineages and form dental cells is needed. However, the study of stem cells requires their isolation and a lack of a specific marker has hindered studies so far.

Researchers in the group of Professor Irma Thesleff at the Institute of Biotechnology in Helsinki, Finland have now found a marker for dental stem cells. They showed that the transcription factor Sox2 is specifically expressed in stem cells of the mouse incisor (front tooth). The mouse incisor grows continuously throughout life and this growth is fueled by stem cells located at the base of the tooth. These cells offer an excellent model to study dental stem cells.

The researchers developed a method to record the division, movement, and specification of these cells. By tracing the descendants of genetically labeled cells, they also showed that Sox2 positive stem cells give rise to enamel-forming ameloblasts as well as other cell lineages of the tooth.

Although human teeth dont grow continuously, the mechanisms that control and regulate their growth are similar as in mouse teeth. Therefore, the discovery of Sox2 as a marker for dental stem cells is an important step toward developing a complete bioengineered tooth. In the future, it may be possible to grow new teeth from stem cells to replace lost ones, says researcher Emma Juuri, a co-author of the study.

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The above story is reprinted from materials provided by Helsingin yliopisto (University of Helsinki), via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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One step closer to growing a tooth

Newswise KANSAS CITY, MO Not all adult stem cells are created equal. Some are busy regenerating worn out or damaged tissues, while their quieter brethren serve as a strategic back-up crew that only steps in when demand shoots up. Now, researchers at the Stowers Institute for Medical Research have identified an important molecular cue that keeps quiescent mouse hematopoietic (or blood-forming) stem cells from proliferating when their services are not needed.

Publishing in the July 20, 2012 issue of Cell, the team led by Stowers Investigator Linheng Li, Ph.D., report that Flamingo and Frizzled 8, a tag team best known for its role in establishing cell polarity, are crucial for maintaining a quiescent reserve pool of hematopoietic stem cells in mouse bone marrow. Their finding adds new insight into the mechanism that controls the delicate balance between long-term maintenance of stem cells and the requirements of ongoing tissue maintenance and regeneration.

Hematopoietic stem cells daily produce billions of blood cells via a strict hierarchy of lineage-specific progenitors, says Li. Identifying the molecular signals that allow hematopoietic stem cell populations to sustain this level of output over a lifetime is fundamental to understanding the development of different cell types, the nature of tumor formation, and the aging process. My hope is that these insights will help scientists make meaningful progress towards new therapies for diseases of the blood.

The current working model, which grew out of earlier work by Li and others, postulates that hematopoietic stem cells (HSC), which are part of the reserve pool sit quietly and only divide a few times a year. They jump into action only when needed to replace active HSCs damaged by daily wear and tear or to increase their numbers in response to injury or disease. But how quiescent and active hematopoietic stem cell subpopulations are maintained and regulated in vivo is largely unknown.

What is known is that both populations of cells reside in adjacent specialized microenvironments, which provide many of the molecular cues that guide stem cell activity. Frequently cycling HSCs constitute around 90 percent of all hematopoietic stem cells and are found in the central marrow, where they seek the company of endothelial and perivascular cells. The main home base of quiescent hematopoietic stem cells is trabecular bone, the spongy part typically found at the end of long bones. Here, these cells engage in a constant molecular dialog with preosteoblasts, the precursors of bone-forming osteoblasts, which are characterized by the expression of N-cadherin.

Trying to decode the nature of the conversation graduate student and first author Ryohichi Sugimura focused on Flamingo (Fmi), a surface-based adhesion molecule, and Frizzled 8 (Fz8), a membrane-based receptor. Both molecules are part of the non-canonical arm of the so-called Wnt signaling pathway, a large network of secreted signaling molecules and their receptors. The canonical arm of the Wnt-signaling pathway exerts its influence through beta-catenin and helps regulate stem cell self-renewal in the intestine and hair follicles.

After in vitro experiments had revealed that Fmi and Fz8 accumulate at the interface between co-cultured quiescent hematopoietic stem cells and preosteoblasts, Sugimura and his colleagues were able to show that Fmi also regulates Fz8 distribution in vivo. This observation provided the first hint that these cooperation partners may carry at least part of the conversation that instructs hematopoietic stem cells to sit still. It also confirmed the previous finding by Lis team that a portion of HSCs resides in the N-cadherin+ osteoblastic niche.

When Sugimura examined the expression patterns of individual members of the Wnt signaling network within quiescent HSCs microenvironment he found that levels of canonical Wnt ligands where low. Levels of non-canonical Wnt ligands and inhibitors of the canonical arm of the Wnt signaling network, on the other hand, were high.

These observations indicated that the osteoblast niche provides a microenvironment in which non-canonical Wnt signaling prevails over canonical Wnt-signaling under normal conditions, says Sugimura. It also suggested that Fmi and Fz8 may play a direct role in maintaining the pool of quiescent hematopoietic stem cells.

Mice that had been genetically engineered to lack either Fmi or Fz8 provided the crucial clue: Not only had the number of quiescent hematopoietic stem cells plummeted in these mice, their hematopoietic stem cell function was reduced by more than 70 percent as well.

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The Yin and Yang of Stem Cell Quiescence and Proliferation

Public release date: 19-Jul-2012 [ | E-mail | Share ]

Contact: Nicole Fawcett nfawcett@umich.edu 734-764-2220 University of Michigan Health System

ANN ARBOR, Mich. Breast cancer treatments such as Herceptin that target a marker called HER2 have dramatically improved outcomes for women with this type of cancer. But nearly half of these cancers are resistant to Herceptin from the start and almost all of them will eventually become resistant.

Now, researchers at the University of Michigan Comprehensive Cancer Center have discovered one reason why the cancer cells become resistant: They turn on a completely different pathway, one that is involved in inflammation, fueling the cancer independently of HER2.

The pathway at work involves a protein called Interleukin-6, or IL-6. The researchers also showed in mice that a drug that blocks IL-6 can stop this effect and overcome the Herceptin resistance.

"Resistance to HER2-targeted therapies remains a major challenge in treating breast cancer. Our study suggests that an IL-6 inhibitor in combination with Herceptin may be a valuable addition for treating HER2-positive breast cancer," says senior study author Max S. Wicha, M.D., Distinguished Professor of Oncology and director of the U-M Comprehensive Cancer Center.

Results of the study will be published in the Aug. 24 issue of Molecular Cell.

Not only are these cells resistant to Herceptin, but they develop higher proportions of cancer stem cells, the small number of cells within a tumor that fuel the growth and spread. This makes the tumor extremely aggressive and likely to spread throughout the body. The IL-6 inhibitor also was shown to prevent this increase in cancer stem cells.

"There is evidence that patients with a lot of IL-6 tend to do poorly. What we found now is that in many of the Herceptin-resistant breast cancers, the IL-6 inflammation loop is driving the cancer stem cell," says lead study author Hasan Korkaya, D.V.M., Ph.D., research assistant professor of internal medicine at the U-M Medical School.

The researchers found that blocking the IL-6 inflammatory loop almost completely blocked the cancer and the stem cells. Mice treated with the IL-6 blocker along with Herceptin immediately after the cancer developed never became resistant to Herceptin.

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Inflammatory pathway spurs cancer stem cells to resist HER2-targeted breast cancer treatment

ScienceDaily (July 18, 2012) New research at the Hebrew University of Jerusalem sheds light on pluripotency -- the ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine.

If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University's Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathways -- which cause biological changes without a corresponding change in the DNA sequence -- that are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an "open" chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell's nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells' differentiation potential," concludes Dr. Meshorer. "This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases."

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Mechanisms that allow embryonic stem cells to become any cell in the human body identified

Public release date: 18-Jul-2012 [ | E-mail | Share ]

Contact: Dov Smith dovs@savion.huji.ac.il 972-258-81641 The Hebrew University of Jerusalem

New research at the Hebrew University of Jerusalem sheds light on pluripotencythe ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine. If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University's Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathwayswhich cause biological changes without a corresponding change in the DNA sequencethat are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an "open" chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell's nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells' differentiation potential," concludes Dr. Meshorer. "This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases."

The research was funded by grants from the European Union (ERC, Marie Curie), Israel Science Foundation, Ministry of Science, Ministry of Health, The National Institute for Psychobiology, Israel Cancer Research Foundation (ICRF), Abisch-Frenkel Foundation and Human Frontiers Science Program (HFSP).

The research appears in the journal Nature Communications as Melcer et al., Histone modifications and lamin A regulate chromatin protein dynamics in early embryonic stem cell differentiation.

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Researchers identify mechanisms that allow embryonic stem cells to become any cell in the human body

ScienceDaily (July 17, 2012) Using adult stem cells, Johns Hopkins researchers and a consortium of colleagues nationwide say they have generated the type of human neuron specifically damaged by Parkinson's disease (PD) and used various drugs to stop the damage.

Their experiments on cells in the laboratory, reported in the July 4 issue of the journal Science Translational Medicine, could speed the search for new drugs to treat the incurable neurodegenerative disease, but also, they say, may lead them back to better ways of using medications that previously failed in clinical trials.

"Our study suggests that some failed drugs should actually work if they were used earlier, and especially if we could diagnose PD before tremors and other symptoms first appear," says one of the study's leaders, Ted M. Dawson, M.D., Ph.D., a professor of neurology at the Johns Hopkins University School of Medicine.

Dawson and his colleagues, working as part of a National Institute of Neurological Disorders and Stroke consortium, created three lines of induced pluripotent stem (iPS) cells derived from the skin cells of adults with PD. Two of the cell lines had the mutated LRKK2 gene, a hallmark of the most common genetic cause of PD. Induced pluripotent stem cells are adult cells that have been genetically reprogrammed to their most primitive state. Under the right circumstances, they can develop into most or all of the 200 cell types in the human body.

In the laboratory, the consortium scientists used the iPS cells to create dopamine neurons, those that bear the brunt of PD. Around age 60, people who have the disorder typically begin to show symptoms, including shaking (tremors) and difficulty with walking, movement and coordination. In the United States, at least 500,000 people are believed to have PD, and an estimated 50,000 new cases are reported annually.

Dawson says the ability to experiment with a form of "Parkinson's in a dish" should lead to further understanding of how the disease originates, develops and behaves in humans. Although scientists have been able to stop the disease in mice, the compounds used to do so have not worked in people, suggesting that human PD behaves differently than animal models of the disorder. Dawson, director of Johns Hopkins' Institute for Cell Engineering, says the researchers began with the belief that PD is strongly linked to disruption of the dopamine neurons' mitochondria, the energy-making power plants of the cells. Mitochondria undergo regular turnover in which they fuse together and then split apart. Normal neurons make new mitochondria and degrade older mitochondria in a balanced way to supply just the amount of energy needed.

PD, Dawson says, is believed to damage this system, leaving too few functional mitochondria and producing too many brain-damaging oxygen-free radicals.

Dawson and his colleagues looked for -- and found -- evidence of impaired mitochondria in the neurons they derived from PD patients.

They also found that the neurons they generated from PD patients were more susceptible to stressors, such as the pesticide rotenone, placed on them in the lab. Those neurons were more likely to become damaged or to die than the neurons derived from the skin of healthy individuals.

Satisfied that their stem cell-generated neurons were behaving like dopamine brain cells, the scientists next set out to see if they could slow the damage occurring in the PD neurons by introducing various compounds to the cells. They tested Coenzyme Q10, rapamycin and the LRRK2 kinase inhibitor GW5074, all of which are known to reverse mitochondrial defects in animals. The cells responded favorably to all three treatments, preventing stressors from continuing to damage the mitochondria.

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Researchers turn skin cells into brain cells, a promising path to better Parkinson's treatment

NEWARK, Calif., July 17, 2012 (GLOBE NEWSWIRE) -- StemCells, Inc. (STEM), today announced preclinical data demonstrating that its proprietary human neural stem cells restored memory and enhanced synaptic function in two animal models relevant to Alzheimer's disease (AD). The data was presented today at the Alzheimer's Association International Conference 2012 in Vancouver, Canada.

The study results showed that transplanting the cells into a specific region of the brain, the hippocampus, statistically increased memory in two different animal models. The hippocampus is critically important to the control of memory and is severely impacted by the pathology of AD. Specifically, hippocampal synaptic density is reduced in AD and correlates with memory loss. The researchers observed increased synaptic density and improved memory post transplantation. Importantly, these results did not require reduction in beta amyloid or tau that accumulate in the brains of patients with AD and account for the pathological hallmarks of the disease.

The research was conducted in collaboration with a world-renowned leader in AD, Frank LaFerla, Ph.D., Director of the University of California, Irvine (UCI) Institute for Memory Impairments and Neurological Disorders (UCI MIND), and Chancellor's Professor, Neurobiology and Behavior in the School of Biological Sciences at UCI. Matthew Blurton-Jones, Ph.D., Assistant Professor, Neurobiology and Behavior at UCI, presented the study results.

"This is the first time human neural stem cells have been shown to have a significant effect on memory," said Dr. LaFerla. "While AD is a diffuse disorder, the data suggest that transplanting these cells into the hippocampus might well benefit patients with Alzheimer's. We believe the outcomes in these two animal models provide strong rationale to study this approach in the clinic and we wish to thank the California Institute of Regenerative Medicine for the support it has given this promising research."

Stephen Huhn, M.D., FACS, FAAP, Vice President and Head of the CNS Program at StemCells, added, "While reducing beta amyloid and tau burden is a major focus in AD research, our data is intriguing because we obtained improved memory without a reduction in either of these pathologies. AD is a complex and challenging disorder. The field would benefit from the pursuit of a diverse range of treatment approaches and our neural stem cells now appear to offer a unique and viable contribution in the battle against this devastating disease."

About Alzheimer's Disease

Alzheimer's disease is a progressive, fatal neurodegenerative disorder that results in loss of memory and cognitive function. Today there is no cure or effective treatment option for patients afflicted by Alzheimer's disease. According to the Alzheimer's Association, approximately 5.4 million Americans have Alzheimer's disease, including nearly half of people aged 85 and older. The prevalence of Alzheimer's disease is expected to increase rapidly as a result of the country's aging population.

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of cell-based therapeutics and tools for use in stem cell-based research and drug discovery. The Company's lead therapeutic product candidate, HuCNS-SC(R) cells (purified human neural stem cells), is currently in development as a potential treatment for a broad range of central nervous system disorders. In a Phase I clinical trial in Pelizaeus-Merzbacher disease (PMD), a fatal myelination disorder in children, the Company has shown preliminary evidence of progressive and durable donor-derived myelination in all four patients transplanted with HuCNS-SC cells. The Company is also conducting a Phase I/II clinical trial in chronic spinal cord injury in Switzerland and recently reported positive interim safety data for the first patient cohort. The Company has also initiated a Phase I/II clinical trial in dry age-related macular degeneration (AMD), and is pursuing preclinical studies in Alzheimer's disease. StemCells also markets stem cell research products, including media and reagents, under the SC Proven(R) brand. Further information about StemCells is available at http://www.stemcellsinc.com.

The StemCells, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=7014

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StemCells, Inc. Announces Its Human Neural Stem Cells Restore Memory in Models of Alzheimer's Disease

Eighteen top science students from northern Wisconsin high schools have earned the opportunity to hone their laboratory skills and work alongside leading researchers from the University of Wisconsin-Madison at a summer science camp focused on stem cells.

Hosted by the Morgridge Institute for Research, a nonprofit biomedical research institute affiliated with UW-Madison, the four-day summer science camp starts today and will cover a number of hands-on activities. Students will participate in neural and cardiac differentiation labs, attend lectures from top UW-Madison researchers and enjoy some time for fun and relaxation at campus attractions including Union South and the Kohl Center.

Students will work with both human embryonic stem cells and induced pluripotent stem cells. Human embryonic stem cells are blank-slate, or pluripotent, cells that have the capacity to differentiate into any of the more than 220 cell types in the human body. Induced pluripotent stem cells derived from reprogrammed skin cells show some differences from human embryonic stem cells and also are the focus of much promising research for human health and pharmaceutical development.

Human embryonic stem cells were first isolated on the UW-Madison campus by James Thomson, who also was among the first to create induced pluripotent stem cells. Today, Wisconsin researchers are considered leaders in developing an understanding of these cells as they search for treatments and cures for diseases such as diabetes, Parkinson's and heart disease. Wisconsin scientists also are pioneering the use of stem cells to help develop better and safer medicines.

Students will use stem cell lines that were established approximately 10 years ago. These cells continue to play a vital role in international research because of their flexibility and well-documented performance characteristics.

The students participating in the camp, held July 16-19, attend schools and educational centers including Cornell High School; Forward Service Corp.; Oconto Falls High School; Oneida Nation High School; and Rhinelander High School. The students earned the honor of attending through their classroom performance and dedication during months of preparatory study.

Students participating in the stem cell camp are:

The stem cell science camp was designed to provide an enrichment experience in an advanced scientific field while introducing promising students to the variety of academic opportunities on the UW-Madison campus.

"Through the camp, we are able to provide students with an in-depth opportunity to broaden their horizons in science, technology and medicine while highlighting the tremendous career opportunities in these rapidly growing fields," says Rupa Shevde, a senior scientist and director of outreach experiences for the Morgridge Institute for Research. "The students benefit from learning about the cutting-edge research that is going on while at the same time gaining hands-on experience with stem cells and other critically important research tools. Introducing the students to stem cells allows us to teach a variety of concepts including the genetic aspects of human diseases and important ethical considerations for researchers."

This summer's stem cell science camp also will feature lectures and presentations from a number of UW-Madison stem cell researchers, including:

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Northern Wisconsin high schoolers learn with stem cells, UW researchers

Public release date: 17-Jul-2012 [ | E-mail | Share ]

Contact: Vanessa McMains vmcmain1@jhmi.edu 410-502-9410 Johns Hopkins Medical Institutions

Johns Hopkins tissue engineers have used tiny, artificial fiber scaffolds thousands of times smaller than a human hair to help coax stem cells into developing into cartilage, the shock-absorbing lining of elbows and knees that often wears thin from injury or age. Reporting online June 4 in the Proceedings of the National Academy of Sciences, investigators produce an important component of cartilage in both laboratory and animal models. While the findings are still years away from use in people, the researchers say the results hold promise for devising new techniques to help the millions who endure joint pain.

"Joint pain affects the quality of life of millions of people. Rather than just patching the problem with short-term fixes, like surgical procedures such as microfracture, we're building a temporary template that mimics the cartilage cell's natural environment, and taking advantage of nature's signals to biologically repair cartilage damage," says Jennifer Elisseeff, Ph.D., Jules Stein Professor of Ophthalmology and director of the Translational Tissue Engineering Center at the Johns Hopkins University School of Medicine.

Unlike skin, cartilage can't repair itself when damaged. For the last decade, Elisseeff's team has been trying to better understand the development and growth of cartilage cells called chondrocytes, while also trying to build scaffolding that mimics the cartilage cell environment and generates new cartilage tissue. This environment is a 3-dimensional mix of protein fibers and gel that provides support to connective tissue throughout the body, as well as physical and biological cues for cells to grow and differentiate.

In the laboratory, the researchers created a nanofiber-based network using a process called electrospinning, which entails shooting a polymer stream onto a charged platform, and added chondroitin sulfatea compound commonly found in many joint supplementsto serve as a growth trigger. After characterizing the fibers, they made a number of different scaffolds from either spun polymer or spun polymer plus chondroitin. They then used goat bone marrow-derived stem cells (a widely used model) and seeded them in various scaffolds to see how stem cells responded to the material.

Elisseeff and her team watched the cells grow and found that compared to cells growing without scaffold, these cells developed into more voluminous, cartilage-like tissue. "The nanofibers provided a platform where a larger volume of tissue could be produced," says Elisseeff, adding that 3-dimensional nanofiber scaffolds were more useful than the more common nanofiber sheets for studying cartilage defects in humans.

The investigators then tested their system in an animal model. They implanted the nanofiber scaffolds into damaged cartilage in the knees of rats, and compared the results to damaged cartilage in knees left alone.

They found that the use of the nanofiber scaffolds improved tissue development and repair as measured by the production of collagen, a component of cartilage. The nanofiber scaffolds resulted in greater production of a more durable type of collagen, which is usually lacking in surgically repaired cartilage tissue. In rats, for example, they found that the limbs with damaged cartilage treated with nanofiber scaffolds generated a higher percentage of the more durable collagen (type 2) than those damaged areas that were left untreated.

"Whereas scaffolds are generally pretty good at regenerating cartilage protein components in cartilage repair, there is often a lot of scar tissue-related type 1 collagen produced, which isn't as strong," says Elisseeff. "We found that our system generated more type 2 collagen, which ensures that cartilage lasts longer."

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Nanoscale scaffolds and stem cells show promise in cartilage repair

Human neural stem cells. Courtesy UC Irvine radiation oncology professor Charles Limoli.

Human neural stem cells restored memory in mice with brain symptoms similar to Alzheimers disease, UC Irvine scientists reported Tuesday, opening the door to eventual treatment for human sufferers.

The announcement, made at an Alzheimers science conference in Vancouver, involves versatile though still largely mysterious neural stem cells grown in the lab by StemCells Inc., of Newark, Ca.

The cells, researchers at UCI and elsewhere have shown, can become many types of cells once injected into the body restoring limb movement in mice with crushed spines, halting blindness in rats and, now, improving memory and brain function in mice bred to exhibit the kinds of impairment seen in Alzheimers.

Youve probably heard about the God particle scientists have been working on, said Martin McGlynn, president and CEO of StemCells Inc. This isnt quite the God cell, but its an incredibly fascinating biological agent.

Over the past 12 to 18 months, scientists including Frank LaFerla, director of UCI MIND, worked on a treatment involving injection of the human neural stem cells into the brains of two kinds of mouse models those bred to model the effects of Alzheimers, and those bred to model the loss of neurons in a part of the brain known as the hippocampus.

Both animal models reported improvement in memory function, in a statistical way, McGlynn said.

Matthew Blurton-Jones, an assistant professor of neurobiology and behavior at UCI, presented the results of the Alzheimers work Tuesday at the Alzheimers Association International Conference.

Part of the scientists aim was to learn whether human neural cells placed in mice functioned as well as mouse neural cells.

That is one of the fascinating things about this, McGlynn said. They look like, smell like, walk like, dance like a human neural stem cell, (but) theyre fully regulated and submissive to the mouse, to the host.

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Stem-cell discovery: reversing Alzheimer's?