2002Zhongguo bingli shengli zazhiRequires access

Role of angiotensin II and angiotensin II receptors in vascular smooth muscle cells migration

Jing Tao

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Abstract

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 .

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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 .

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Available abstract

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 .

Key concepts: Angiotensin II, Vascular smooth muscle, Antagonist, Motility, Cytoskeleton, Angiotensin II receptor type 1, Cell biology, Receptor

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