Low-level mechanical strain induces extracellular signal-regulated kinase 1/2 activation in alveolar epithelial cells

Background and objective: The pattern and the degree of mechanical stimuli may determine cellular responses, but little is known about how low magnitude stimuli are converted into biochemical signals in alveolar epithelial cells (AEC). The aim of this study was to explore whether extracellular signal-regulated kinases 1/2 (ERK1/2) are activated by low-level strain in A549 cells and how mechanical factors affect ERK1/2 phosphorylation. Methods: A549 cells (an AEC line) were exposed to cyclic tensile strain via a four-point bending system, with strains of different magnitude (437, 874, 1748, 3496 µstrain), duration (5, 15, 30, 60, 120 min) and frequency (0.5, 1 Hz). Phosphorylation of ERK1/2 proteins was assessed by western blot. Results: Maximal ERK1/2 phosphorylation occurred in the 874 µstrain group (a 2.25-fold increase, P