ARB affects nicotine-induced gene expression profile in human coronary artery endothelial cells  

作　　者：Masataka Kudo Ken Matsuda Kaori Sugawara Yuko Iki Naotaka Kogure Takako Saito-Ito Kyoko Shimizu Ikuko Sato Takeo Yoshikawa Akira Uruno Ryo Ito Atsushi Yokoyama Akiko Saito-Hakoda Sadayoshi Ito Akira Sugawara 

机构地区：[1]Division of Nephrology,Endocrinology,and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan [2]Department of Molecular Endocrinology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan [3]Department of Pharmacology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan [4]Department of Medical Biochemistry,Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan

出　　处：《World Journal of Hypertension》2014年第1期7-14,共8页世界高血压杂志

基　　金：Supported by Grants from Smoking Research Foundation(to Sugawara A)

摘　　要：AIM: To investigate the effects of nicotine and nicotine plus angiotensin Ⅱ receptor blocker(ARB) on the gene expression profile of human coronary artery endothelial cells(HCAECs).METHODS: The changes in gene expression profiles in HCAECs treated with nicotine and nicotine plus ARB olmesartan were analyzed by DNA microarray. In nicotine-treated HCAECs, 432 genes selected by P < 0.01 were greater than 1.5-fold compared with the untreated cells. Data were analyzed using IPA(Ingenuity? Systems, www.ingenuity.com).RESULTS: The gene expression levels of tumor necrosis factor-α, collagen type 1, matrix metalloproteinase-10, and disintegrin and metalloprotease domain 8, which are related to "cardiovascular function and disease", were significantly increased. In canonical pathway analyses using IPA, "atherosclerosis signaling" was strongly affected by nicotine treatment and this effect was reduced by co-incubation with ARB olmesartan. These data indicate that the deleterious cardiovascular consequences of cigarette smoking may, at least in part, be due to the nicotine-induced gene expression profile related to "atherosclerosis signaling".CONCLUSION: The inhibitory effect of ARB against the nicotine-induced gene expression profile may possibly induce anti-atherosclerotic effects that are independent of those from lowering the blood pressure.AIM: To investigate the effects of nicotine and nicotine plus angiotensin Ⅱ receptor blocker(ARB) on the gene expression profile of human coronary artery endothelial cells(HCAECs).METHODS: The changes in gene expression profiles in HCAECs treated with nicotine and nicotine plus ARB olmesartan were analyzed by DNA microarray. In nicotine-treated HCAECs, 432 genes selected by P < 0.01 were greater than 1.5-fold compared with the untreated cells. Data were analyzed using IPA(Ingenuity? Systems, www.ingenuity.com).RESULTS: The gene expression levels of tumor necrosis factor-α, collagen type 1, matrix metalloproteinase-10, and disintegrin and metalloprotease domain 8, which are related to "cardiovascular function and disease", were significantly increased. In canonical pathway analyses using IPA, "atherosclerosis signaling" was strongly affected by nicotine treatment and this effect was reduced by co-incubation with ARB olmesartan. These data indicate that the deleterious cardiovascular consequences of cigarette smoking may, at least in part, be due to the nicotine-induced gene expression profile related to "atherosclerosis signaling".CONCLUSION: The inhibitory effect of ARB against the nicotine-induced gene expression profile may possibly induce anti-atherosclerotic effects that are independent of those from lowering the blood pressure.

关 键 词：AngiotensinⅡ Atherosclerosis Microarray OLMESARTAN SMOKING 

分 类 号：R[医药卫生]