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Updated: Aug 25, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Mechanical pressure-induced phosphorylation of p38 mitogen-activated protein kinase in epithelial cells via Src and
Matthias Hofmann1, Julijana Zaper, August Bernd
1Department of Dermatology and Venerology, University Hospital, Johann Wolfgang Goethe-University, D-60590 Frankfurt/Main, Germany.
Abstract:
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/cm(2)) 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.
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