期刊
FASEB JOURNAL
卷 23, 期 9, 页码 3089-3099出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.09-130237
关键词
myoblast; dystrophin; transplantation; receptor; EpoR
资金
- National Institute of Diabetes and Digestive and Kidney Diseases
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.-Jia, Y., Warin, R., Yu, X., Epstein, R., Noguchi, C. T. Erythropoietin signaling promotes transplanted progenitor cell survival. FASEB J. 23, 3089-3099 ( 2009). www.fasebj.org
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据