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首页> 外文期刊>Journal of pharmacological sciences. >Nicotinic Acetylcholine Receptor alpha7 Subunit Mediates Migration of Vascular Smooth Muscle Cells Toward Nicotine.
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Nicotinic Acetylcholine Receptor alpha7 Subunit Mediates Migration of Vascular Smooth Muscle Cells Toward Nicotine.

机译:烟碱乙酰胆碱受体α7亚基介导血管平滑肌细胞向尼古丁的迁移。

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摘要

GbaSM-4 cells, vascular smooth muscle cells (VSMCs) derived from brain basilar arteries, were shown to migrate toward d-nicotine by augmenting the actin cytoskeleton in their cell bodies and lamellipodia, and expression of nicotinic acetylcholine receptor (alpha7-nAChR) was detected in GbaSM-4 cells. Their chemotaxis was antagonized by an alpha7-nAChR antagonist of methyllycaconitine. It was also antagonized by inhibiting myosin light chain (MLC) kinase and by down-regulating MLC kinase. However, the changes in MLC phosphorylation were not associated with the nicotine treatment, suggesting the involvement of non-kinase activity of MLC kinase as reviewed by Gao et al. (IUBMB Life. 2001;51:337). This plot may work to induce arteriosclerosis during cigarette smoking.
机译:GbaSM-4细胞是源自脑基底动脉的血管平滑肌细胞(VSMC),通过增加其肌体中的肌动蛋白细胞骨架和lamellipodia而向d-尼古丁迁移,而尼古丁乙酰胆碱受体(alpha7-nAChR)的表达为在GbaSM-4细胞中检测到。它们的趋化性被甲基卡可尼丁的α7-nAChR拮抗剂拮抗。它也通过抑制肌球蛋白轻链(MLC)激酶和下调MLC激酶而被拮抗。但是,MLC磷酸化的变化与尼古丁的治疗无关,这提示了高(Gao)等人综述了MLC激酶的非激酶活性。 (IUBMB Life。2001; 51:337)。该情节可能在吸烟过程中诱发动脉硬化。

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