{"title":"Role of Angiotensin II Subtype 1 Receptor in Smooth Muscle Cells Apoptosis after Balloon Injury to Vessel","authors":"Geng M. Wang, G. He, Xiao-hui Xu, GUO-CHAO Wang","doi":"10.55503/2790-6744.1465","DOIUrl":null,"url":null,"abstract":"ET AL.: Role of Angiotensin II Subtype 1 Receptor in Smooth Muscle Cells Apoptosis after Balloon Injury to Vessel. In order to investigate the mechanism of smooth muscle cells apoptosis after balloon injury to vessel, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and immunohistochemistry were adopted to measure the percentage of vascular smooth muscle cell (VSMC) apoptosis and the expression of angiotensin II subtype 1 receptor (AT 1 R). Compared with sham's, the expression of AT 1 R protein in vascular media was significantly increased at 3 days after balloon injury (P<0.05), and then did not change significantly . At 7 days, it was approximately twice in intima as that in media. At 28 days it reached its peak. VSMCs apoptosis occurred in vascular media at 3 days after balloon injury and reached a peak in media and intima where apoptosis was mainly present at 7 days, then decreased. At 28 days after balloon injury, only a few apoptotic cells were in intima. AT 1 R antagonist (irbesartan) significantly increased VSMCs apoptosis. We thus conclude that AT 1 R is upregulated after balloon injury and angiotensin II inhibits VSMC apoptosis by binding to AT 1 R. (J HK Coll Cardiol 2000;8:49-57) Angiotensin II, receptor, vascular smooth muscle, apoptosis","PeriodicalId":53534,"journal":{"name":"Journal of the Hong Kong College of Cardiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the Hong Kong College of Cardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.55503/2790-6744.1465","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
ET AL.: Role of Angiotensin II Subtype 1 Receptor in Smooth Muscle Cells Apoptosis after Balloon Injury to Vessel. In order to investigate the mechanism of smooth muscle cells apoptosis after balloon injury to vessel, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and immunohistochemistry were adopted to measure the percentage of vascular smooth muscle cell (VSMC) apoptosis and the expression of angiotensin II subtype 1 receptor (AT 1 R). Compared with sham's, the expression of AT 1 R protein in vascular media was significantly increased at 3 days after balloon injury (P<0.05), and then did not change significantly . At 7 days, it was approximately twice in intima as that in media. At 28 days it reached its peak. VSMCs apoptosis occurred in vascular media at 3 days after balloon injury and reached a peak in media and intima where apoptosis was mainly present at 7 days, then decreased. At 28 days after balloon injury, only a few apoptotic cells were in intima. AT 1 R antagonist (irbesartan) significantly increased VSMCs apoptosis. We thus conclude that AT 1 R is upregulated after balloon injury and angiotensin II inhibits VSMC apoptosis by binding to AT 1 R. (J HK Coll Cardiol 2000;8:49-57) Angiotensin II, receptor, vascular smooth muscle, apoptosis
血管紧张素II亚型1受体在血管球囊损伤后平滑肌细胞凋亡中的作用。为了探讨血管球囊损伤后平滑肌细胞凋亡的机制,采用末端脱氧核苷酸转移酶介导的dUTP生物素缺口末端标记(TUNEL)和免疫组织化学方法检测血管平滑肌细胞(VSMC)凋亡百分比和血管紧张素II亚型1受体(AT1R)的表达。与假手术组相比,球囊损伤后3d血管介质中AT1R蛋白的表达显著增加(P<0.05),但无明显变化。在第7天,内膜中的表达量大约是中膜中表达量的两倍。第28天达到高峰。球囊损伤后第3天,VSMCs在血管介质中出现凋亡,第7天,VSMC在以凋亡为主的介质和内膜中达到峰值,然后逐渐减少。球囊损伤后28天,内膜中仅有少量凋亡细胞。AT1R拮抗剂(厄贝沙坦)显著增加VSMCs凋亡。因此,我们得出结论,球囊损伤后AT1R上调,血管紧张素II通过与AT1R结合抑制VSMC凋亡。(J HK Coll Cardiol 2000;8:49-57)血管紧张素Ⅱ,受体,血管平滑肌,细胞凋亡
期刊介绍:
The Journal of the Hong Kong College of Cardiology publishes peer-reviewed articles on all aspects of cardiovascular disease, including original clinical studies, review articles and experimental investigations. As official journal of the Hong Kong College of Cardiology, the journal publishes abstracts of reports to be presented at the Scientific Sessions of the College as well as reports of the College-sponsored conferences.