Xue-Qing Jin1, Zhuo-Qiang Lu, Xu Lin. 1. Hypertension Research Division, Department of Cardiology, First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China. jxueqing@sohu.com
Abstract
OBJECTIVE: To investigate the effect of AngII on the proliferation of vascular smooth muscle cell (VSMC) in rats after the transfection of ACE2 gene. METHODS: pm-ACE2 was transfected into the cultured VSMC by Lipofectamine 2000. The normal cell group, AngIIgroup and pcDNA3.1/Hygro(+) transfected + AngII group were taken as controls respectively. After the transfection of ACE2 gene, the cell proliferative effect of AngII on VSMC was investigated by cell counting kit-8 (CCK8) and cell cycle detection by fluorescence activated cell sorter (FACS). RESULTS: The (optical density) OD value of AngIIgroup was obviously higher than that of other groups. And it was obviously lower in the pm-ACE2 + AngII group than the AngII group (0.535 ± 0.004 vs 0.866 ± 0.026, P < 0.05). Compared with other groups, the G(0)/G(1) stage percentage of VSMC was obviously lower in the AngII group (58.80% ± 2.00%, P < 0.05) while the percentage of S stage was obviously higher (35.90% ± 1.00%, P < 0.05). Compared with the AngII group, the G(0)/G(1) stage percentage of VSMC was obviously higher (63.90% ± 1.40%, P < 0.05) in the pm-ACE2 + AngII group while the percentage of S stage was obviously lower (27.80% ± 0.46%, P < 0.05). CONCLUSION: The over-expression of ACE2 gene can inhibit the proliferation of AngII-induced VSMC.
OBJECTIVE: To investigate the effect of AngII on the proliferation of vascular smooth muscle cell (VSMC) in rats after the transfection of ACE2 gene. METHODS: pm-ACE2 was transfected into the cultured VSMC by Lipofectamine 2000. The normal cell group, AngIIgroup and pcDNA3.1/Hygro(+) transfected + AngII group were taken as controls respectively. After the transfection of ACE2 gene, the cell proliferative effect of AngII on VSMC was investigated by cell counting kit-8 (CCK8) and cell cycle detection by fluorescence activated cell sorter (FACS). RESULTS: The (optical density) OD value of AngIIgroup was obviously higher than that of other groups. And it was obviously lower in the pm-ACE2 + AngII group than the AngII group (0.535 ± 0.004 vs 0.866 ± 0.026, P < 0.05). Compared with other groups, the G(0)/G(1) stage percentage of VSMC was obviously lower in the AngII group (58.80% ± 2.00%, P < 0.05) while the percentage of S stage was obviously higher (35.90% ± 1.00%, P < 0.05). Compared with the AngII group, the G(0)/G(1) stage percentage of VSMC was obviously higher (63.90% ± 1.40%, P < 0.05) in the pm-ACE2 + AngII group while the percentage of S stage was obviously lower (27.80% ± 0.46%, P < 0.05). CONCLUSION: The over-expression of ACE2 gene can inhibit the proliferation of AngII-induced VSMC.