拉伸通过蛋白激酶诱导肺泡细胞的生长因子

Hiroyuki Yamamoto, Hidemi Teramoto, Kohsaku Uetani, Katsutoshi Igawa, Eiji Shimizu
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引用次数: 47

摘要

正压机械通气可损伤肺,引起水肿和肺泡炎症,并发症称为呼吸机诱导肺损伤(VILI)。据报道,白细胞介素-8 (IL-8)等细胞因子在这种炎症反应中很重要。另一方面,肝细胞生长因子(HGF)促进肺再生,延缓肺纤维化。我们假设循环拉伸上调这两种介质的产生和释放。体外循环拉伸后,检测体外培养的人肺泡上皮细胞(A549) mRNA的表达及IL-8和HGF的释放。拉伸诱导这些介质的mRNA表达和释放。从循环拉伸到IL-8和HGF释放的信号通路似乎涉及蛋白激酶C在信号转导通路中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stretch induces a growth factor in alveolar cells via protein kinase

Positive-pressure mechanical ventilation can injure the lung, causing edema and alveolar inflammation in a complication termed ventilator-induced lung injury (VILI). Cytokines such as interleukin-8 (IL-8) reportedly are important in this inflammatory response. On the other hand, hepatocyte growth factor (HGF) promotes regeneration of the lung, and delays pulmonary fibrosis. We postulated that cyclic stretch upregulates production and release of both of mediators. Human alveolar epithelial cells (A549) cultured on a silicoelastic membrane were tested for mRNA expression and release of IL-8 and HGF after cyclic stretch in vitro. Stretch induced mRNA expression and release of these mediators. The signaling pathway from cyclic stretch to release of IL-8 and HGF appeared to involve protein kinase C in the signal transduction pathway.

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