Li Sheng, Zhao Tiejun, Xin Hong, Ye Li-Hong, Zhang Xiaodong, Tanaka Hideyuki, Nakamura Akio, Kohama Kazuhiro
Department of Molecular and Cellular Pharmacology, Faculty of Medicine, Gunma University Graduate School of Medicine, Japan.
J Pharmacol Sci. 2004 Mar;94(3):334-8. doi: 10.1254/jphs.94.334.
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.
GbaSM - 4细胞，即源自脑基底动脉的血管平滑肌细胞（VSMCs），通过增强其细胞体和片状伪足中的肌动蛋白细胞骨架，显示出向d - 尼古丁迁移，并且在GbaSM - 4细胞中检测到烟碱型乙酰胆碱受体（α7 - nAChR）的表达。它们的趋化性被甲基lycaconitine的α7 - nAChR拮抗剂所拮抗。通过抑制肌球蛋白轻链（MLC）激酶和下调MLC激酶也可拮抗其趋化性。然而，MLC磷酸化的变化与尼古丁处理无关，这表明如Gao等人综述的那样，MLC激酶的非激酶活性参与其中（IUBMB Life. 2001;51:337）。这种情况可能在吸烟过程中促使动脉粥样硬化的发生。
