Abstract
Pulmonary epithelial cells are exposed to mechanical strain during physiological breathing and mechanical ventilation. It was not clear which style was more related with cell mechanotransduction. c-fos is known to be a component of a transcription factor, activator protein-1, which is induced by oxidative stress. The regulatory pathways involved in the rapid response of the AP-1 transcription factor, c-fos, to mechanical load in the human pulmonary epithelial cell line A549 were investigated using a four-point bending model. In an effort to better understand what processes are involved in mechanotransduction, we have examined whether and how soon c-fos induction occurs in human A549 shortly after the application of the different mechanical strains stimuli.
Published Version
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