The role of focal adhesion kinase in the TGF-β-induced myofibroblast transdifferentiation of human Tenon's fibroblasts.

摘要: Myofibroblast transdifferentiation of activated fibroblasts is an essential step the fibrotic process in most living tissues. Myofibroblasts have characteristics that are taken from both smooth muscle cells and fibroblasts; they express contractile phenotype α actin (αSMA) synthesize extracellular matrix proteins including collagens [1-3]. In subconjunctival fibrosis, myofibroblast Tenon's known to be mainly caused by transforming growth factor (TGF)-β [4-6]. Many ophthalmic researchers sought identify anti-fibrotic mechanism inhibiting TGF-β signaling [7-10]. Focal adhesion kinase (FAK), a cytosolic protein tyrosine kinase, provides scaffolding functions at sites integrin promotes cell migration [11,12]. The modulates several basic processes normal development cancer metastasis. addition, it also plays crucial role myofibroblasts induced [13-15]. However, because precise action somewhat variable based on tissue [14,15], FAK human must confirmed. Using primary cultured fibroblasts, TGF-β-induced was investigated present study.