作者: Yuan-Hung Chao , Yang-Hwei Tsuang , Jui-Sheng Sun , Cheng-Kung Cheng , Ming-Hong Chen
DOI: 10.3109/03008207.2010.525673
关键词:
摘要: Ultrasound is an effective noninvasive treatment for various tendinopathies. However, how tenocytes convert ultrasound stimulation into cascades of cellular and molecular events not well understood. The purpose this study to elucidate the signaling pathways during stimulation. Primary cultures were harvested from Achilles tendons Sprague-Dawley rats. viability proliferation tenocytes, their genes expression, after with or without specific inhibitors evaluated analyzed. results showed that (100 mW/cm(2) 20 min) significantly enhanced matrix metalloproteinase 13 (MMP-13), c-Fos, c-Jun gene increased JNK p38, but extracellular signal-regulated kinase-1/2 (ERK1/2), phosphorylation at 5 min, sustained up 60 min. inhibitor p38 inhibitor, ERK1/2 attenuated ultrasound-dependent induction MMP-13 indicating are required ultrasound-induced expression in tenocytes. We also found SB431542 (transforming growth factor-beta (TGF-β) receptor kinases inhibitor) suppressed MMP?13 c-Fos phosphorylation. This revealed stimulates regulates metabolism through cross-talk between TGF-β mitogen-activated protein (MAPKs) pathways.