Posts tagged muscle tissue
Articles and news from the latest research reports.
Researchers Find Dying Cells Essential to Muscle Development and Repair
Dying cells play an unexpected and vital role in the creation of muscle fibers, researchers at the University of Virginia School of Medicine have determined. The finding could lead to new ways to battle conditions such as muscular dystrophy, facilitate healing after surgery and benefit athletes in their efforts to recover more quickly.
“These dead cells aren’t just a nuisance, which we’ve always considered them to be,” U.Va.’s Kodi S. Ravichandran said. “They have other, important roles before they leave this world.”
Dying cells have long been considered debris that must be removed from the body to avoid causing tissue inflammation. However, the U.Va. research shows that a small number of myoblasts – precursor cells that develop into muscle tissue – must die to allow muscle formation.
The finding suggests that programmed cell death, known as apoptosis, can also influence differentiation of other healthy cells within a tissue. The dying cells express a marker on their surface that signals their death and spurs the body to remove them; that same marker on these dying cells, the U.Va. researchers discovered, cues surrounding cells to develop into muscle fibers. The U.Va. researchers have identified both the membrane marker on the dying cells (a lipid normally hidden on live cells) and a corresponding receptor in the healthy myoblasts that are induced to fuse, said Ravichandran, chairman of the School of Medicine’s Department of Microbiology, Immunology and Cancer Biology.
“It’s been known for a while that there are a few muscle cells that die during exercise, and that building muscle mass depends on a few of those cells dying,” Ravichandran said. “This work puts an interesting spin on that.”
The discovery opens up many intriguing avenues for researchers to explore, including the possibility of producing muscle growth either through the direct application of apoptotic cells or by otherwise stimulating the cellular signaling pathways on the healthy cells. The genes encoding the receptor protein (called BAI1) and some of the components of the signaling pathway are found to be altered in patients with muscular dystrophy and other forms of muscle disorders.
“Because this pathway seems to be involved in muscle repair after injury, this could be relevant for recovery after surgeries, combat injuries in soldiers or any condition that could lead to muscle injury or muscle atrophy,” Ravichandran said. “Take Duchenne muscular dystrophy, for example. One in 3,500 boys that are born have this disease. If we can help alleviate the distress of even a few of these individuals, we would have made significant progress.”
The findings have been published online by the journal Nature and will appear in a forthcoming print edition (along with a News and Views highlighting the impact of the work).
(Source: news.virginia.edu)
Discovering ‘Needle in a Haystack’ For Muscular Dystrophy Patients
Muscular dystrophy is caused by the largest human gene, a complex chemical leviathan that has confounded scientists for decades. Research conducted at the University of Missouri and described this month in the Proceedings of the National Academy of Sciences has identified significant sections of the gene that could provide hope to young patients and families.
MU scientists Dongsheng Duan, PhD, and Yi Lai, PhD, identified a sequence in the dystrophin gene that is essential for helping muscle tissues function, a breakthrough discovery that could lead to treatments for the deadly hereditary disease. The MU researchers “found the proverbial needle in a haystack,” according to Scott Harper, PhD, a muscular dystrophy expert at The Ohio State University who is not involved in the study.
Duchenne muscular dystrophy (DMD), predominantly affecting males, is the most common type of muscular dystrophy. Children with DMD face a future of rapidly weakening muscles, which usually leads to death by respiratory or cardiac failure before their 30th birthday.
Patients with DMD have a gene mutation that disrupts the production of dystrophin, a protein essential for muscle cell survival and function. Absence of dystrophin starts a chain reaction that eventually leads to muscle cell degeneration and death. While dystrophin is vital for muscle development, the protein also needs several “helpers” to maintain the muscle tissue. One of these “helper” molecular compounds is nNOS, which produces nitric oxide that can keep muscle cells healthy during exercise.
"Dystrophin not only helps build muscle cells, it’s also a key factor to attracting nNOS to the muscle cell membrane, which is important during exercise," Lai said. "Prior to this discovery, we didn’t know how dystrophin made nNOS bind to the cell membrane. What we found was that dystrophin has a special ‘claw’ that is used to grab nNOS and bring it to the muscle cell membrane. Now that we have that key, we hope to begin the process of developing a therapy for patients."
Another Muscular Dystrophy Mystery Solved; MU Scientists Inch Closer to a Therapy for Patients
Approximately 250,000 people in the United States suffer from muscular dystrophy, which occurs when damaged muscle tissue is replaced with fibrous, bony or fatty tissue and loses function. Three years ago, University of Missouri scientists found a molecular compound that is vital to curing the disease, but they didn’t know how to make the compound bind to the muscle cells. In a new study, published in the Proceedings of the National Academies of Science, MU School of Medicine scientists Yi Lai and Dongsheng Duan have discovered the missing pieces to this puzzle that could ultimately lead to a therapy and, potentially, a longer lifespan for patients suffering from the disease.
Duchenne muscular dystrophy (DMD), predominantly affecting males, is the most common type of muscular dystrophy. Patients with Duchenne muscular dystrophy have a gene mutation that disrupts the production of dystrophin, a protein essential for muscle cell survival and function. Absence of dystrophin starts a chain reaction that eventually leads to muscle cell degeneration and death. While dystrophin is vital for muscle development, the protein also needs several “helpers” to maintain the muscle tissue. One of these “helper” molecular compounds is nNOS, which produces nitric oxide that can keep muscle cells healthy after exercise.
“Dystrophin not only helps build muscle cells, it’s also a key factor to attracting nNOS to the muscles cells and helping nNOS bind to the cell and help repair it following activity,” said Lai, a research assistant professor in the Department of Molecular Microbiology and Immunology. “Prior to this discovery, we didn’t know how dystrophin made nNOS bind to the cells. What we found was that dystrophin has a special ‘claw’ that is used to grab nNOS and bring it close to the muscle cell. Now that we have that key, we hope to begin the process of developing a therapy for patients.”
Neural-Like Stem Cells From Muscle Tissue May Hold Key to Cell Therapies for Neurodegenerative Diseases
Scientists at Wake Forest Baptist Medical Center have taken the first steps to create neural-like stem cells from muscle tissue in animals. Details of the work are published in two complementary studies published in the September online issues of the journals Experimental Cell Research and Stem Cell Research.
“Reversing brain degeneration and trauma lesions will depend on cell therapy, but we can’t harvest neural stem cells from the brain or spinal cord without harming the donor,” said Osvaldo Delbono, M.D., Ph.D., professor of internal medicine at Wake Forest Baptist and lead author of the studies.
“Skeletal muscle tissue, which makes up 50 percent of the body, is easily accessible and biopsies of muscle are relatively harmless to the donor, so we think it may be an alternative source of neural-like cells that potentially could be used to treat brain or spinal cord injury, neurodegenerative disorders, brain tumors and other diseases, although more studies are needed.”
In an earlier study, the Wake Forest Baptist team isolated neural precursor cells derived from skeletal muscle of adult transgenic mice (PLOS One, Feb.3, 2011).
In the current research, the team isolated neural precursor cells from in vitro adult skeletal muscle of various species including non-human primates and aging mice, and showed that these cells not only survived in the brain, but also migrated to the area of the brain where neural stem cells originate.
Another issue the researchers investigated was whether these neural-like cells would form tumors, a characteristic of many types of stem cells. To test this, the team injected the cells below the skin and in the brains of mice, and after one month, no tumors were found.
“Right now, patients with glioblastomas or other brain tumors have very poor outcomes and relatively few treatment options,” said Alexander Birbrair, a doctoral student in Delbono’s lab and first author of these studies. “Because our cells survived and migrated in the brain, we may be able to use them as drug-delivery vehicles in the future, not only for brain tumors but also for other central nervous system diseases.”
In addition, the Wake Forest Baptist team is now conducting research to determine if these neural-like cells also have the capability to become functioning neurons in the central nervous system.
(Source: newswise.com)