Muscle stem cells, the cells in muscle fibers that generate new muscle cells after injury or exercise, lose their potency with age. But a study by researchers at Stanford Medicine shows that old mice regain the leg muscle strength of younger animals after receiving an antibody treatment that targets a pathway mediated by a molecule called CD47.
The findings are surprising because CD47, billed as the “don’t eat me” molecule, is better known as a target for cancer immunotherapy than for muscle regeneration. It peppers the surface of many cancer cells, protecting them from immune cells that patrol the body to root out and engulf dysfunctional or abnormal cells. Now it seems old muscle stem cells may use a similar approach to avoid being culled by the immune system… Continue reading.
Regenerative medicine could hold the keys to rejuvenating older muscles, and research supporting that will be featured at the Mayo Clinic Symposium on Regenerative Medicine and Surgery. Preclinical research by Helen Blau, Ph.D., Stanford University School of Medicine, discovered a protein that triggers muscle loss and a way to block it to restore youthful muscle strength. Dr. Blau, director of the Baxter Laboratory for Stem Cell Biology at Stanford University School of Medicine, will present her research in a virtual keynote speech… Continue reading.
In her laboratory in Barcelona, Spain, Miki Ebisuya has built a clock without cogs, springs or numbers. This clock doesn’t tick. It is made of genes and proteins, and it keeps time in a layer of cells that Ebisuya’s team has grown in its lab. This biological clock is tiny, but it could help to explain some of the most conspicuous differences between animal species.
Animal cells bustle with activity, and the pace varies between species. In all observed instances, mouse cells run faster than human cells, which tick faster than whale cells. These differences affect how big an animal gets, how its parts are arranged and perhaps even how long it will live. But biologists have long wondered what cellular timekeepers control these speeds, and why they vary… Continue reading.
For well over a decade now, scientists have been experimenting with “couch potato” drugs that could confer the benefits of exercise without having to flex a muscle. The latest candidate is a small molecule inhibitor impeding the degradation of prostaglandin E2 (PGE2), recently shown to act directly on mature muscle fibers to prevent deleterious molecular changes that arise with aging, according to Helen Blau, professor of microbiology and immunology and director of the Baxter Laboratory for Stem Cell Biology at Stanford University School of Medicine.
In gel form, PGE2 is already being used to induce labor and treat respiratory distress in newborns, says Blau. It now appears that restoring PGE2 later in life could be a way to rejuvenate aging muscles and possibly treat conditions such as age-related muscle atrophy (sarcopenia), Duchenne muscular dystrophy, and other myopathies… Continue reading.
Treatments are lacking for sarcopenia, a debilitating age-related skeletal muscle wasting syndrome. We identifed increased amounts of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), the prostaglandin E2 (PGE2)-degrading enzyme, as a hallmark of aged tissues, including skeletal muscle. The consequent reduction in PGE2 signaling contributed to muscle atrophy in aged mice and results from 15-PGDH-expressing myofibers and interstitial cells, such as macrophages, within muscle. Overexpression of 15-PGDH in young muscles induced atrophy. Inhibition of 15-PGDH, by targeted genetic depletion or a small-molecule inhibitor, increased aged muscle mass, strength, and exercise performance. These benefits arise from a physiological increase in PGE2 concentrations, which augmented mitochondrial function and autophagy and decreased transforming growth factor-β signaling and activity of ubiquitin-proteasome pathways. Thus, PGE2 signaling ameliorates muscle atrophy and rejuvenates muscle function, and 15-PGDH may be a suitable therapeutic target for countering sarcopenia… Continue reading.
Blocking the activity of a single protein in old mice for one month restores mass and strength to the animals’ withered muscles and helps them run longer on a treadmill, according to a study by researchers at the Stanford University School of Medicine. Conversely, increasing the expression of the protein in young mice causes their muscles to atrophy and weaken.
“The improvement is really quite dramatic” said Helen Blau, PhD, professor of microbiology and immunology. “The old mice are about 15% to 20% stronger after one month of treatment, and their muscle fibers look like young muscle. Considering that humans lose about 10% of muscle strength per decade after about age 50, this is quite remarkable… Continue reading.
WASHINGTON, D.C.—The American Institute for Medical and Biological Engineering (AIMBE) has announced the induction of Helen M. Blau, Ph.D., Donald E. and Delia B. Baxter Foundation Professor and Director, Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, to its College of Fellows.
Election to the AIMBE College of Fellows is among the highest professional distinctions accorded to a medical and biological engineer. The College of Fellows is comprised of the top two percent of medical and biological engineers. College membership honors those who have made outstanding contributions to “engineering and medicine research, practice, or education” and to “the pioneering of new and developing fields of technology, making major advancements in traditional fields of medical and biological engineering, or developing/implementing innovative approaches to bioengineering education.”
Dr. Blau was nominated, reviewed, and elected by peers and members of the College of Fellows for “seminal contributions in the use of bioengineered materials to advance stem cell biology and regenerative medicine.”