The mechanism by which excessive stretching induces gene expressions and protein production of inflammatory mediators in cultured human pulmonary artery endothelial cells

本研究的目的是阐明在周期性拉伸条件下，拉伸诱导正常人肺动脉内皮细胞(HPAEC)炎性介质表达的机制，以及类PEEP周期拉伸对IL-6蛋白产生的影响。诱导基因表达的候选途径的起点是周期性拉伸改变细胞内的钙离子浓度。过度循环拉伸可产生IL-6蛋白，但类PEEP循环拉伸显著抑制IL-6蛋白的产生。在机械通气过程中，即使细胞过度伸展，PEEP也会对HPAEC产生保护作用。

The aims of this study were to elucidate the mechanism by whichstretching induces expression of inflammatory mediators in normal human pulmonary artery endothelial cells (HPAEC) when subjected to cyclic stretching, and to examine theeffects of PEEP-like cyclic stretch on the IL-6 protein production. The starting point of candidate pathways inducing gene expressions is Ca2+ concentration in the cells changed by cyclic stretching. The IL-6 protein was produced by excessive cyclic stretching, but its production was significantly suppressed by PEEP-like cyclic stretching. HPAECswould be protected by PEEP during mechanical ventilation even if the cells are excessively stretched.