Sci. Signal., 10 December 2013
Inhibiting Muscle Repair During InflammationWhen skeletal muscle cells become injured, they secrete the inflammatory cytokine interferon- (IFN-), which is required for the fusion of myoblasts to form new myofibers that repair the damaged tissue; however, excess IFN- represses muscle repair. Londhe and Davie found that IFN- inhibited the expression of muscle-specific genes in cultured mouse muscle cells through a mechanism involving the sequential recruitment of the class II transactivator (CIITA) and repressor proteins of the Jumonji and Polycomb families. Mice subjected to muscle injury and a mouse model of muscular dystrophy, which exhibits excess IFN- in muscle, had increased amounts of Polycomb proteins in their muscle fibers compared to those of wild-type mice. Together, these data suggest that IFN- recruits repressor proteins to muscle-specific genes to inhibit muscle differentiation during inflammation.
Citation: P. Londhe, J. K. Davie, Interferon- Resets Muscle Cell Fate by Stimulating the Sequential Recruitment of JARID2 and PRC2 to Promoters to Repress Myogenesis. Sci. Signal. 6, ra107 (2013).
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