Scientists at UMDNJ-Robert Wood Johnson Medical School are a step closer to treating, and perhaps preventing, muscle damage caused by neurodegenerative disorders and other forms of disease. In a newly published study, released April 19 and cited as a Paper of the Week by the Journal of Biological Chemistry, the team has discovered that the gene polymerase I and transcript release factor, or PTRF, is an essential component of the cell process that repairs damaged muscle tissue.
This discovery has the potential to lead to development of therapeutic treatment for patients who suffer from severe complications of diseases such as muscular dystrophy, cardiovascular disorders and other degenerative conditions.
The research was led by Jianjie Ma, PhD, professor and acting chair of physiology and biophysics at UMDNJ-Robert Wood Johnson Medical School. Hua Zhu, PhD, an instructor in Dr. Ma's laboratory, is the first author on the manuscript describing this discovery.
According to Dr. Ma, human cells are continuously injured and naturally repaired throughout their life span. For instance, micro tears can occur as muscles contract within the body during normal everyday activities. However, diseases such as diabetes, cardiovascular disorders and muscular dystrophy, and even aging, compromise the method through which the body repairs its own tissues, resulting in severe damage. His research team announced in December 2008 that it had discovered MG53 as a key initiator of membrane repair in damaged tissue, making it the first group to specifically pinpoint a protein responsible for promoting cell repair.
In this new study, the team's research has revealed that in order for MG53 to successfully repair damaged tissue, it must work cooperatively with PTRF. During the muscle repair process PTRF acts as a docking protein, potentially binding MG53 with exposed membrane cholesterol at the injury site. When PTRF is absent in cells, the binding process is interrupted and MG53 can not successfully repair damaged tissues.
"The identification of PTRF as a molecule that anchors MG53 to injured tissue will help us to better understand how a cell membrane can repair itself," said Dr. Ma. "The discovery of PTRF as a necessary component in the initiation of muscle repair is another hopeful step toward the development of therapeutic treatments for patients with muscle and cardiovascular disease."
The research was supported by grants from the National Institutes of Health.
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