Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026850 (muscular dystrophy)
 5,870 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myogenic regulatory factors (MRFs) promote differentiation of muscle cells from fibroblasts and are induced by insulin-like growth factor I (IGF-1). Prior studies have shown synthesis of new muscle protein and improved muscle morphology when mature dy mice with muscular dystrophy are treated with IGF-1. We investigated whether these salutary effects of IGF-1 might be attributable to stimulation of MRFs. Male dy (129ReJ) mice and controls (129J) were assigned to IGF-1 treatment (10 micrograms twice daily) or non-treatment at about 5 weeks of life and sacrificed 6 weeks later. RNA was extracted from skeletal muscles, reverse transcribed, and amplified by polymerase chain reaction (PCR) using primers specific for each MRF. Competitive PCR was performed to quantify MyoD expression in response to IGF-1 treatment. Transcripts for myf-5, MRF4, and myogenin were detected in both control and dy mouse muscles; no apparent differences were observed between treatment groups. Quantitative analysis of transcripts for MyoD indicated no significant basal differences between control and dy mice. There was, however, significantly higher MyoD expression in the dy group, and a trend toward significance in the control group, following IGF-1 treatment. These data suggest that IGF-1 exerts its in vivo effects in postembryonal muscle by stimulating MRFs.
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PMID:Expression of myogenic regulatory factors in normal and dystrophic mice: effects of IGF-1 treatment. 916 95

We examine the potential for erythropoietin signaling to promote donor cell survival in a model of myoblast transplantation. Expression of a truncated erythropoietin receptor in hematopoietic stem cells has been shown to promote selective engraftment in mice. We previously demonstrated expression of endogenous erythropoietin receptor on murine myoblasts, and erythropoietin treatment can stimulate myoblast proliferation and delay differentiation. Here, we report that enhanced erythropoietin receptor expression, as well as exogenous erythropoietin treatment in myoblasts, provided a survival advantage and protection against apoptosis under serum-starvation conditions. When cultured in differentiation medium, expression of the myogenic regulatory proteins shifted toward early differentiation with increased erythropoietin receptor. Expression of early myogenic differentiation proteins Myf-5 and MyoD increased, while later stage protein myogenin decreased. Transplantation of C2C12 myoblasts overexpressing truncated erythropoietin receptor showed more transplanted cell incorporation into muscle fibers in muscular dystrophy mdx mice. These cells also restored dystrophin protein expression in mdx mice at 6 wk after cell treatment that was further increased with exogenous erythropoietin administration. In summary, enhanced erythropoietin receptor expression promotes transplanted cell survival in a mouse model for myoblast transplantation and provides dystrophin expression in mice with muscular dystrophy.
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PMID:Erythropoietin signaling promotes transplanted progenitor cell survival. 1941 86