Myofibroblasts protect myoblasts from intrinsic apoptosis associated with differentiation via β1 integrin-PI3K/Akt pathway.

摘要: Skeletal myoblasts withdrawing from cell cycle is a prerequisite for myodifferentiation, while upon proliferation/differentiation transformation, large portion of will undergo apoptosis. fibroblasts, residing in muscle tissue both during and post myogenesis, have been proofed to play pivotal roles development, their effect on myoblast apoptosis being coincident with differentiation has not reported. Using membrane insert co-culture system, we studied it found that the mitochondrial pathway played crucial role differentiation, fibroblasts promoted only withdrawal but also survival paracrine fashion, which was coupled upregulations β1 integrin, phosphorylated Akt anti-apoptotic protein Bcl2. To determine integrin process, transfected siRNA specific before knockdown abolished ability inhibited activation Bcl2 expression. Blockage PI3K/Akt wortmannin seriously impaired protective fibroblast-induced The data demonstrated protected intrinsic associated integrin-PI3K/Akt required process.