Mechanical stress facilitates calcium influx and growth of alveolar epithelial cells via activation of the BDKRB1/Ca2+/CaMKII/MEK1/ERK axis

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Mechanical stress and calcium metabolism are associated with lung development and various pulmonary diseases. Our previous research demonstrated that BDKRB1/Ca 2+ signal transduction may be involved in lung dysplasia resulting from scoliosis and thoracic insufficiency. Therefore, the present study aims to investigate the effects of mechanical stress on the growth and calcium influx in alveolar epithelial cells, as well as the role of BDKRB1/Ca 2+ signaling in these processes. Flow cytometry, CCK-8, and EDU staining assay were employed to assess the cycle, calcium influx, activity, and proliferation in RLE-6TN cells subjected to mechanical stresses of varying amplitudes (5%, 10% and 15%). RT-qPCR and western blotting assay were performed to evaluate the effects of mechanical stress on BDKRB1/Ca 2+ /CaMKII/MEK1/ERK signaling in RLE-6TN cells. Mechanical stress at 10% amplitudes effectively enhanced the viability, EDU positive ratio, S-phase percentage, and Ca 2+ concentration of RLE-6TN cells, while reducing the G1-phase percentage. Conversely, 15% mechanical stress exerted an inhibitory effect on RLE-6TN cell proliferation. Additionally, 10% mechanical stress significantly upregulated the expression of BDKRB1, CaMKIIα/δ, p-MEK1 and p-ERK1/2 in RLE-6TN cells. Notably, BDKRB1 knockdown attenuated the 10% mechanical stress-induced increase in both growth and calcium influx in RLE-6TN cells. Moreover, BDKRB1 knockdown blocked the activation of the Ca 2 ⁺/CaMKII/MEK1/ERK pathway induced by 10% mechanical stress. Appropriate levels of mechanical stress contribute to the growth and calcium influx of alveolar epithelial cells by modulating BDKRB1/Ca 2+ /CaMKII/MEK1/ERK signaling.

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