by Amy Adams on July 16, 2010 at 2:05PM | comments
Stanford scientists have overcome one significant hurdle in developing a therapy for muscle-wasting diseases like muscular dystrophy. Until now, the muscle stem cells that stand at the ready to repair muscle damage couldn't be grown outside the safe confines of a muscle. Once uprooted from their home and transferred to a laboratory dish, they matured into less useful progenitor cells. That's a problem because once mature the cells no longer have the potential to be transplanted to repair muscle damaged by injury or disease.
by Amy Adams on February 10, 2010 at 2:26PM | comments
Stem cells in fat hold intrigue for scientists because most of us have excess to spare, and the cells seem to be quite versatile. Now a team at Stanford has found a way to transform them into induced pluripotent stem (iPS) cells without using potentially dangerous viruses to carry the reprogramming genes into the cells.
by Amy Adams on January 27, 2010 at 2:46PM | comments
Induced pluripotent stem (iPS) cells have created excitement and head scratching ever since they were first created a little over two years ago. The excitement arises from their creation through reprogramming adult cells by manipulating their gene function, which does not require a human embryo and could potentially give a patient personalized replacement cells. But determining just how identical they are to embryonic stem cells in function has caused much consternation.
by Amy Adams on October 1, 2009 at 8:34AM | comments
Researchers at the University of California, Berkeley have found molecular pathways that human muscle stem cells rely on to repair damaged muscle. These pathways are active in younger people but less active in older people, explaining why muscles repair more slowly with age. The group found that younger volunteers had double the number of regenerative muscle stem cells in their thigh muscles compared to older volunteers. After two weeks in a leg cast, both groups began exercise routines to rebuild muscle.
by Amy Adams on July 24, 2009 at 12:13PM | comments
Researchers at the University of California, Irvine have reversed Alzheimer's-like symptoms in a mouse model of the disease with injections of neural stem cells. The mice used in this study mimicked the human disease, showing learning and memory defects and accumulating both beta-amyloid plaques and tau protein tangles within the brain, the two hallmark pathologies of the disease. Mice that received injections of mouse neural stem cells performed significantly better in memory tests than mice that received control injections. The stem cells did not replace cells lost to the disease.
by Amy Adams on July 8, 2009 at 12:12PM | comments
Researchers at the University of California, San Francisco have pinpointed a protein that is critical for maintaining a stem cell's full potential to self-renew and to differentiate. Stem cells lacking the protein were impaired in their ability to divide and make identical copies of themselves, called self-renewal. These cells also lost their capacity to differentiate into key cell types, such as cardiac muscle. The protein, Chd1, acts to keep chromosome strands loosely wound, which permits widespread gene activation in the cell's nucleus.
by Amy Adams on July 5, 2009 at 12:10PM | comments
Researchers at the Gladstone Institute of Cardiovascular Disease have identified two molecules, called microRNAs, that push early heart cells to mature into the smooth muscle cells that line blood vessels. These same molecules also control when those smooth muscle cells divide to repair damage or in diseases such as cancer or atherosclerosis, which both involve unhealthy blood vessel growth. The two microRNAs, miR-145 and miR-143, are abundant in the primitive heart cells of prenatal mice, leading those cells to differentiate into various mature heart and aorta cells.
by Amy Adams on May 23, 2009 at 12:09PM | comments
Researchers at the University of California, Irvine have found that neurons derived from embryonic stem cells were able to repair some damage in a mouse model of multiple sclerosis. In people with MS, the immune system attacks the insulation â called myelin â that covers and protects neurons of the brain and spinal cord. The transplanted cells caused a response in the animals that allowed the myelin coating to be repaired on damaged cells. In humans, repairing the myelin would likely also repair the function of those nerves, bringing back feeling and motor control in people with MS.