Mechanical pressure-induced phosphorylation of p38 mitogen-activated protein kinase in epithelial cells via Src and protein kinase C

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• 作者：Hofmann ; Matthias ; Zaper ; Julijana ; Bernd ; August ; Bereiter-Hahn ; Jü ; rgen ; Kaufmann ; Roland ; et. al.
• 关键词：Mechanical pressure ; Epithelial cells ; p38 ; PKC ; Src
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2004
• 出版时间：April 9, 2004
• 年：2004
• 卷：316
• 期：3
• 页码：673-679
• 全文大小：1.14 M

文摘

Mechanical stimulation is known to modulate cell physiology in a variety of different tissues. Particularly, epithelial cells are permanently exposed to mechanical stimulation generated by externally applied forces. The present in vitro study demonstrated mechanical pressure as a trigger-factor of the p38 mitogen-activated protein kinase (MAPK) pathway in epithelial cells. Mechanical pressure applied by teflon weights (1.02g/cm²) led to a rapid phosphorylation of p38 peaking between 5 and 10min. Furthermore, phosphorylation of the small heat shock protein 27 (HSP27) was shown in response to mechanical pressure. Suppression of p38 function by using specific inhibitors blocked the pressure-mediated phosphorylation of HSP27. In order to identify upstream regulators of p38, a contribution of Src and protein kinase C (PKC) in pressure-signaling was investigated. We could demonstrate that inhibition of Src or PKC suppressed the pressure-induced phosphorylation of p38. These findings suggest mechanical pressure as a new type of effector stimulus for the p38 pathway with implications to (patho-) physiological conditions.