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拉伸诱导正常人肺动脉内皮细胞（HPAEC）在循环拉伸时炎症介质表达的机制，并研究peep样循环拉伸对IL-6蛋白产生的影响。诱导基因表达的候选途径的起点是细胞内Ca2+浓度的循环拉伸变化。IL-6蛋白是通过过度循环拉伸产生的，但其产生被peep样循环拉伸明显抑制。在机械通气期间，即使细胞过度拉伸，hpaecs也会受到PEEP的保护。

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.