Transforming growth factor-beta1-induced satellite cell apoptosis in chickens is associated with beta1 integrin-mediated focal adhesion kinase activation.

Transforming growth factor-beta1 (TGF-beta1) induces apoptosis in many types of cells. The cell adhesion receptor, beta1 integrin subunit, prevents apoptosis and may be involved in TGF-beta1-induced muscle cell apoptosis. In the current study, chicken primary satellite cells, myogenic precursors, were used to investigate the apoptotic effect of TGF-beta1 on muscle cells. The data from the current study showed that the addition of exogenous TGF-beta1 reduced beta1 integrin expression and altered its localization. Treatment of the satellite cells with TGF-beta1 increased the number of apoptotic cells indicated by annexin-V using flow cytometry. The number of caspase-positive cells was increased in the TGF-beta1-treated immunostained cells, which supported that TGF-beta1 induced satellite cell apoptosis. It has been shown that beta1 integrin is involved in muscle cell survival. In response to the activation of beta1 integrin, focal adhesion kinase (FAK) phosphorylates tyrosine at residue 397 and activates cell survival signal transduction. The phosphorylation of FAK was significantly reduced from 30 min to 4 h after TGF-beta1 treatment during both satellite cell proliferation and differentiation. These data suggested that the apoptotic effect of TGF-beta1 on satellite cells is likely associated with a beta1 integrin-mediated FAK signaling pathway during satellite cell proliferation and differentiation.