Monthly Archives: April 2012

New Stem Cell Found in the Brain

 Researchers at Lund University in Sweden have discovered a new stem cell in the adult brain. These cells can proliferate and form several different cell types — most importantly, they can form new brain cells. Scientists hope to take advantage of the finding to develop methods to heal and repair disease and injury in the brain.

Analyzing brain tissue from biopsies, the researchers for the first time found stem cells located around small blood vessels in the brain. The cell’s specific function is still unclear, but its plastic properties suggest great potential.

“A similar cell type has been identified in several other organs where it can promote regeneration of muscle, bone, cartilage and adipose tissue,” said Patrik Brundin, M.D., Ph.D., Jay Van Andel Endowed Chair in Parkinson’s Research at Van Andel Research Institute (VARI), Head of the Neuronal Survival Unit at Lund University and senior author of the study.

In other organs, researchers have shown clear evidence that these types of cells contribute to repair and wound healing. Scientists suggest that the curative properties may also apply to the brain. The next step is to try to control and enhance stem cell self-healing properties with the aim of carrying out targeted therapies to a specific area of the brain.

“Our findings show that the cell capacity is much larger than we originally thought, and that these cells are very versatile,” said Gesine Paul-Visse, Ph.D., Associate Professor of Neuroscience at Lund University and the study’s primary author. “Most interesting is their ability to form neuronal cells, but they can also be developed for other cell types. The results contribute to better understanding of how brain cell plasticity works and opens up new opportunities to exploit these very features.”

The study, published in the journal PLoS ONE, is of interest to a broad spectrum of brain research. Future possible therapeutic targets range from neurodegenerative diseases to stroke.

“We hope that our findings may lead to a new and better understanding of the brain’s own repair mechanisms,” said Dr. Paul-Visse. “Ultimately the goal is to strengthen these mechanisms and develop new treatments that can repair the diseased brain.”

 

Source: Health News

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Scientists Engineer Stem Cells That Can Identify and Destroy HIV Inside Living Mice

Genetically engineered human stem cells have been shown to be capable of suppressing HIV by virus-infected cells in living mice, according to scientists who hope that the recent breakthrough will lead to a cure for HIV patients. 

Previous HIV research largely focused on vaccines or drugs that aim to slow the virus’s progression, but the latest findings offers hope of a potential treatment that can completely eradicate HIV from an infected patient, according to researchers from the latest study published April 12 in the journal PLoS Pathogens.

“We believe that this study lays the groundwork for the potential use of this type of an approach in combating HIV infection in infected individuals, in hopes of eradicating the virus from the body,” lead researcher Scott G. Kitchen, an assistant professor of medicine in the division of hematology and oncology at the David Geffen School of Medicine at University of California, Los Angeles said in a statement.

Previously, scientists took CD8 cytotoxic T lymphocytes or “killer” T cells that fight infections from HIV patients and identified the molecule that guides the T cells in recognizing and killing HIV-infected cells.

While these HIV-destroying cells exist in the body, they are not in great enough quantities to eradicate the virus from the body, according to researchers.

After identifying the molecule, researchers cloned the receptor and used it to genetically engineer human blood stem cells that were placed into human thymus tissue that had been implanted in mice, which allowed them to observe the reaction in a living animal model.

Past findings show that the engineered stem cells developed into a large population of mature, multi-functional HIV-specific CD8 cells that could specifically attack cells containing HIV proteins.

However, researcher noted that HIV-specific T cell receptors need to be matched to an individual which is similar to how an organ is matched to a transplant patient.

Researchers from the current study replicated previously engineered human blood stem cells and placed them in a surrogate mouse model, in which HIV infection resembles the disease and progression in humans.

Afterwards, researchers conducted a series of tests on the mice’s peripheral blood, plasma and organs two weeks and six weeks after introducing the genetically engineered cells and discovered that the previously depleting number of CD4 “helper” T cells, white blood cells that help fight off infections, actually increased and levels of HIV in the blood decreased.

While the latest research has for the first time provided evidence that engineered cells were capable of developing and migrating to the organs to fight infection there, researchers noted that because human immune cells reconstruct at a lower level in genetically engineered “humanized” mice, which had immune systems that were mostly reconstructed, than they would in humans, the virus may mutate slower in mice than in human hosts.

They suggest that a potential way to address this limitation would be to use multiple engineered T cell receptors to adjust for the higher potential for HIV mutation in humans.

“We believe that this is the first step in developing a more aggressive approach in correcting the defects in the human T cell responses that allow HIV to persist in infected people,” Kitchen said.

Researchers are currently working on developing T cell receptors that can be used in more genetically matched individuals and that will be capable of targeting different parts of the virus.

Via Christine HSU, Medical Daily


Stem Cell Treatment Spurs Cartilage Growth

 A small molecule dubbed kartogenin encourages stem cells to take on the characteristics of cells that make cartilage, a new study shows. And treatment with kartogenin allowed many mice with arthritis-like cartilage damage in a knee to regain the ability to use the joint without pain.

The findings provide new clues in the long-running effort to find ways to regenerate cartilage, a central puzzle in the battle against osteoarthritis, scientists report online April 5 in Science.

The new approach taps into mesenchymal stem cells, which naturally reside in cartilage and give rise to cells that make connective tissue. These include chondrocytes, the only cells in the body that manufacture cartilage. Kartogenin steers the stem cells to wake up and take on cartilage-making duties. This is an essential step in the cartilage repair that falls behind in people with osteoarthritis, the most common kind of arthritis, which develops from injury or long-term joint use.

“In the blue-sky scenario, this would be a locally delivered therapy that would target stem cells already there,” says study coauthor Kristen Johnson, a molecular biologist at the Genomics Institute of the Novartis Research Foundation in San Diego.

Johnson and her colleagues screened 22,000 compounds in cartilage and found that one, kartogenin, induced stem cells to take on the characteristics of chondrocytes. The molecule turned on genes that make cartilage components called aggrecan and collagen II. Tests of mice with cartilage damage similar to osteoarthritis showed that kartogenin injections lowered levels of a protein called cartilage oligomeric matrix protein. People with osteoarthritis have an excess of the protein, which is considered a marker of disease severity. Kartogenin also enabled mice with knee injuries to regain weight-bearing capacity on the joint within 42 days.

Lab work revealed that kartogenin inhibits a protein called filamin A in the mesenchymal stem cells. This unleashes other compounds that can then orchestrate the activity of genes useful in turning the stem cells into functional chondrocytes. In so doing, Johnson says, kartogenin seems to protect and repair cartilage.

Millions of people develop osteoarthritis as they reach old age. Cartilage serves as the shock absorber of the skeleton, but surgery to clean out torn cartilage has limited success, as does surgery to induce growth of a fibrous kind of coating at the ends of bones that have lost their natural cartilage caps. This losing battle leaves bone-on-bone friction, inflammation and pain.

“Our cartilage wasn’t meant to live this long,” says molecular biologist Mary Goldring of Weill Cornell Medical College in New York. A cartilage imbalance results from wear and tear, literally, as people age, she says. Regenerating the cartilage-making process in the body has become a primary goal in orthopedic medicine.

Source: Nathan Seppa, Science News