Stem Cell Research Demonstrates Hope for Slowing Age-Related Cellular Degeneration

By Theresa Sangram

Researchers at the University of California, Berkley are setting the path for research on new treatments for age-related degenerative conditions such as muscle atrophy, Alzheimer’s Disease and Parkinson’s Disease. In a recent study published in the journal Nature, researchers used mice to identify two key regulatory pathways that control how well adult stem cells repair and replace damaged tissue. Then, they tweaked how those stem cells reacted to biochemical signals that enhanced the ability of muscle tissue in older mice to repair itself nearly as well as younger mice..

Irina Conboy, an assistant professor of bioengineering and an investigator at the Berkley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), led the research team conducting this study.

The research findings related to adult stem cells residing in existing tissue. This approach to rejuvenating degenerating muscle eliminates the ethical and medical complications associated with transplanting tissues grown from embryonic stem cells. Researchers said that the stem cells in old tissue are still ready and able to perform their regenerative function if they receive the appropriate chemical signals. Studies have shown that when old tissue is placed in an environment of young blood, the stem cells behave as if they are young again.

“We are one step closer to having a point of intervention where we can rejuvenate the body’s own stem cells so we don’t have to suffer from some of the debilitating diseases associated with aging,” said the study’s lead author, Morgan Carlson, a recent Ph.D. graduate of Conboy’s lab.

The researchers focused on the interplay of two competing molecular pathways that control the stem cells. When the aging muscle cells are damaged or worn out, stem cells are called into action to begin the process of rebuilding them.

Adult stem cells have a receptor called “Notch” that, when activated, tells them it is time to grow and divide. However, stem cells also receive a protein (TGF-beta) that sets off a chain reaction that ultimately produces cyclin-dependent kinase (CDK) inhibitors, which limits the cell’s ability to divide. Aging and cellular death are, in part, due to the progressive decline of Notch and the increased levels of TGF-beta which limit the stem cell’s capacity to effectively rebuild the body.

In the study, researchers compared the muscle regeneration capacity of 2-year-old mice, comparable in age to a 75-to-80-year-old human, with that of 2-month-old mice, similar in age to a 20-to-25-year-old human. Researchers found that muscle tissue in the younger mice easily replaced damaged cells with new, healthy cells. In contrast, the areas of damaged muscle in the control group of older mice were characterized by fibroblasts and scar tissue. However, the muscles in the old mice showed levels of cellular regeneration that were comparable to their much younger peers and that were 3 to 4 times greater than those of the group of “untreated” older mice.

Source: Morgan E. Carlson, Michael Hsu, and Irina M. Conboy. 2008. Imbalance between pSmad3 and Notch induces CDK inhibitors in old muscle stem cells. Nature (Advance Online Publication, June 15th)

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