期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 299, 期 5, 页码 C939-C947出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00253.2010
关键词
Wnt3a; beta-catenin; collagen; myopathy; Sca1
资金
- Canadian Institutes of Health Research (CIHR)
- Canada Foundation for Innovation (CFI)
- Fonds de la Recherche en Sante du Quebec (FRSQ)
- FORMSAV
- Fondation pour la Recherche et l'Enseignement en Orthopedie de Sherbrooke (FREOS)
Trensz F, Haroun S, Cloutier A, Richter MV, Grenier G. A muscle resident cell population promotes fibrosis in hindlimb skeletal muscles of mdx mice through the Wnt canonical pathway. Am J Physiol Cell Physiol 299: C939-C947, 2010. First published September 1, 2010; doi: 10.1152/ajpcell.00253.2010.-Previous work has pointed to a role for the Wnt canonical pathway in fibrosis formation in aged skeletal muscles. In the present study, we studied the dystrophic mdx mouse, which displays skeletal muscle fibrosis. Our results indicated that the muscle resident stromal cell (mrSC) population in the muscles of dystrophic mice is higher than in the muscles of age-matched wild-type mice. Wnt3a promoted the proliferation of and collagen expression by cultured mrSCs but arrested the growth of and collagen expression by cultured myoblasts. Injections of Wnt3A in the tibialis anterior muscles of adult wild-type mice significantly enhanced the mrSC population and collagen deposition compared with the contralateral muscles. Conversely, an injection of the Wnt antagonist Dickkof protein (DKK1) into the skeletal muscles of mdx mice significantly reduced collagen deposition. These results suggested that the Wnt canonical pathway expands the population of mrSCs and stimulates their production of collagen as observed during aging and in various myopathies.
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