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

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.

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 microstrain), duration (5, 15, 30, 60, 120 min) and frequency (0.5, 1 Hz). Phosphorylation of ERK1/2 proteins was assessed by western blot.

Maximal ERK1/2 phosphorylation occurred in the 874 microstrain group (a 2.25-fold increase, P < 0.01). In this group, the peak response occurred after 30 min of exposure and slowly decreased to baseline after 90 min. Static strain did not produce a statistically significant increase in ERK1/2 phosphorylation, whereas a frequency of 0.5 Hz produced a 4.56-fold increase compared with the control (P < 0.05). A 10.87-fold increase in response with frequency of 1 Hz was found.

Low-level strain activates ERK1/2 in A549 cells. ERK1/2 may be the key signalling molecules mediating strain-induced cellular responses.