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作 者:景涛[1] 何国祥[1] 刘建平[1] 王耿[1] 吴昊[1] 王海东[2]
机构地区:[1]第三军医大学西南医院心内科,重庆400038 [2]第三军医大学西南医院胸心外科,重庆400038
出 处:《中国病理生理杂志》2002年第2期143-146,共4页Chinese Journal of Pathophysiology
摘 要:目的 :探讨血管紧张素II (AngII)及其受体 (ATRs)在局部血管损伤后血管平滑肌细胞 (VSMC)迁移中的作用及其机制。方法 :以体外培养VSMC为基础 ,采用细胞化学和改良Boyden’schamber的方法 ,观察AngⅡ干预VSMC后AngII受体的表达、VSMC迁移能力的变化、肌动蛋白纤维丝的动态组装变化 ,并探讨AT1R拮抗剂、AT2 R拮抗剂对上述观测指标的影响。结果 :AngII 10 -7mol/L可以刺激VSMC发生迁移 ,该作用是通过影响VSMC内应力纤维动态组装而实现的 ;AngII干预VSMC后可使AT1R表达上调 ,随着作用时间延长AT1R表达水平下降。AT1R拮抗剂可下调AT1R表达。AngII通过AT1R的介导发挥其影响VSMC迁移能力的生物学效应。AT2 R对此无明显影响。结论 :AngII通过AT1R介导来调节VSMC内肌动蛋白微丝的动态组装 ,进而改变VSMC的迁移能力 。AIM: To determine the effects of Angiotensin II(AngII) on migration of rat smooth muscle cells and to investigate the mechanisms underlying Ang II action in the development of injured vascular disease. METHODS: VSMCs isolated from aortic media of Wistar rats and cultured by the modified explant method were adopted. In prersence and absence of AngII, the expression of AngII receptor and reorganization of the actin cytoskeleton of VSMCs were studied by immunocytochemistry technique, fluorocytochemistry technique. The migration assays were performed by a modified Boyden's chamber. And the effects of AT 1R antagonist (CV-11974), AT 2R antagonist (PD123319) on aforementioned target were studied. RESULTS: VSMCs migration was stimulated by addition of AngII. The dynamic reorganization of actin cytoskeleton may be an important mechanism by which AngII facilitates VSMC motility. The expression of AT 1R in VSMCs can be upregulated after treatment with AngII initially, then decreased gradually. The expression of AT 1R was downregulated by AT 1R antagonist. The effect of AngII on VSMCs migration was mediated by AT 1R, while AT 2R had no significant effect. CONCLUSION: The dynamic reorganization of actin cytoskeleton is required for AngII-induced VSMC migration, and this effect is mediated by AT 1R .
关 键 词:血管紧张素Ⅱ 肌细胞 血管紧张素受体 血管平滑肌
分 类 号:R331.32[医药卫生—人体生理学]
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