ラット血管平滑筋の伸展刺激誘導性細胞死における一酸化窒素合成酵素の保護作用

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  • iNOS protects vascular smooth muscle cells from cell death stimulated by cyclic mechanical stretch via the p38 signal pathway.

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<p>Cyclic mechanical stretch (CMS) leads to vascular smooth muscle cells proliferation, cell death and migration, resulting in vascular remodeling and subsequent vascular failure. However, the effect of CMS on gene induction in cardiovascular diseases remains to be determined. We have revealed that CMS caused cell death in rat aortic smooth muscle cells (RASMCs) in JNK and p38-dependent manners. To explore the causal role of CMS in initiating cell death signaling and MAPKs events, we compared transcript profiles of CMS-induced RASMCs death using cDNA microarrays. Inducible nitric oxide synthase (iNOS) gene was identified as having significantly differential expression in response to CMS. We further identified using qPCR analysis that CMS induced iNOS expression in a p38-dependent manner in RASMCs. The result also showed that NO production was increased, implying that NO was synthesized by CMS-induced iNOS. In contrast, NO production was inhibited by p38 inhibitor. Moreover, a iNOS inhibitor strongly increased CMS-induced cell death; whereas a NO donor significantly inhibited CMS-induced cell death in RASMCs, indicating that iNOS protects RASMCs from CMS-stimulated cell death via the p38 signal pathway.</p>

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