Investigate the mechanism of angiotensin Ⅱ induced aortic dissection based on G protein signaling modulator 2 knockout
10.19405/j.cnki.issn1000-1492.2024.07.012
- VernacularTitle:基于G蛋白信号调节因子2敲低探讨血管紧张素Ⅱ诱导的主动脉夹层形成的机制
- Author:
Qinggong WANG
1
;
Yaping XUE
;
Haixia SUN
;
Ning CAO
Author Information
1. 青海省人民医院心血管超声室,西宁 810007
- Keywords:
regulator of G protein signaling 2;
angiotensin Ⅱ;
aortic dissection;
vascular smooth muscle cells
- From:
Acta Universitatis Medicinalis Anhui
2024;59(7):1188-1194
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of G protein signal regulator 2(RGS2)in regulating the formation of angiotensin Ⅱ(Ang Ⅱ)-induced aortic dissection.Methods C57BL/6 mice were divided into 3 groups:control group(n=10),Ang Ⅱ group(n=20),Ang Ⅱ+sh-RGS2 group(n=20).The Ang Ⅱ group and Ang Ⅱ+sh-RGS2 group established an aortic dissection model.The incidence of aortic dissection was evaluated in vivo,and the phenotypic transformation of VSMC was evaluated in vitro and in vivo.Results Knockdown of RGS2 largely coun-teracted Ang Ⅱ-induced inhibition of αSMA,ACTA2 and MYH11,and suppressed Ang Ⅱ-induced SPP1 and Vim-entin in VSMC.The incidence of aortic dissection in Ang Ⅱ group and Ang Ⅱ+sh-RGS2 group were 45％(9/20)and 10％(2/20),respectively.Fewer elastic lamina thickening,aortic rupture,and aortic wall collagen fiber con-tent were observed in Ang Ⅱ+sh-RGS2 group compared to Ang Ⅱ group.In addition,compared with the Ang Ⅱgroup,the maximum diameter of the aorta in the Ang Ⅱ+sh-RGS2 group was significantly reduced(P＜0.05).In addition,the ACTA2 and MYH11 proteins in the aorta of the Ang Ⅱ+sh-RGS2 group were significantly higher than those in the Ang Ⅱ group(P＜0.01),while the RGS2,SPP1,and Vimentin proteins significantly decreased(P＜0.01).Conclusion Knockdown of RGS2 inhibits the transformation of Ang Ⅱ-induced VSMC from a contractile phenotype to a synthetic phenotype,thereby reducing the incidence of aortic dissection formation.
- Full text:202409140911572062基于G蛋白信号调节因子2敲...诱导的主动脉夹层形成的机制_王庆功.pdf
