Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway

Introduction The renin-angiotensin system is associated with blood pressure regulation, inflammation, oxidative stress and insulin resistance. It can decrease intracellular oxidative stress. Stimulation with H 2 O 2 leads to increased oxidative stress and activation of the AKT/mTOR pathway. However...

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Autores principales:	Xuekun Shi, Yuhua Guan, Shaoyan Jiang, Tiandong Li, Bing Sun, Huan Cheng
Formato:	article
Lenguaje:	EN
Publicado:	Termedia Publishing House 2018
Materias:	apoptosis oxidative stress renin-angiotensin system inhibitor akt/mtor pathway endothelial cell dysfunction Medicine R
Acceso en línea:	https://doaj.org/article/41de30315c8f433fa7c4c5fcc3ec009c
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spelling	oai:doaj.org-article:41de30315c8f433fa7c4c5fcc3ec009c2021-12-02T16:58:24ZRenin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway1734-19221896-915110.5114/aoms.2018.74026https://doaj.org/article/41de30315c8f433fa7c4c5fcc3ec009c2018-12-01T00:00:00Zhttps://www.archivesofmedicalscience.com/Renin-angiotensin-system-inhibitor-attenuates-oxidative-stress-induced-human-coronary,82972,0,2.htmlhttps://doaj.org/toc/1734-1922https://doaj.org/toc/1896-9151Introduction The renin-angiotensin system is associated with blood pressure regulation, inflammation, oxidative stress and insulin resistance. It can decrease intracellular oxidative stress. Stimulation with H 2 O 2 leads to increased oxidative stress and activation of the AKT/mTOR pathway. However, the role of renin-angiotensin system inhibitors in oxidative stress-induced endothelial cell dysfunction and H 2 O 2 -induced AKT activation remains unclear. Material and methods Human coronary artery endothelial cells (HCAECs) were used. The cells were treated with H 2 O 2 , captopril, the AKT inhibitor MK-2206, and the AKT activator SC79, either separately, or in combination. p53 and ICAM-1 expression, and p-eNOS, p-Akt and mTOR activation were measured by Western blot. Cell viability was assessed by MTT assay. Levels of reactive oxygen species (ROS) were assayed by flow cytometry. Proliferation was monitored by BrdU labeling, while cell migration and invasion were determined by wound healing and Transwell assays, respectively. Results The renin-angiotensin system inhibitor captopril reversed H 2 O 2 -induced oxidative stress and apoptosis in HCAECs. Co-treatment with captopril and the AKT inhibitor MK-2206 reduced the H 2 O 2 -induced P53 and ICAM-1 protein expression (p < 0.05). The proliferation, migration and invasion of HCAECs were significantly enhanced by co-treatment with captopril and MK-2206 (p < 0.05). Conclusions The study revealed the protective effect of captopril against H 2 O 2 -induced endothelial cell dysfunction through the AKT/mTOR pathway, and its enhancement of cell survival. These findings provide new insights into the protective effects of captopril and novel therapeutic approaches to treatment of cardiovascular disease.Xuekun ShiYuhua GuanShaoyan JiangTiandong LiBing SunHuan ChengTermedia Publishing Housearticleapoptosisoxidative stressrenin-angiotensin system inhibitorakt/mtor pathwayendothelial cell dysfunctionrenin-angiotensin system inhibitoroxidative stressapoptosisendothelial cell dysfunctionMedicineRENArchives of Medical Science, Vol 15, Iss 1, Pp 152-164 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	apoptosis oxidative stress renin-angiotensin system inhibitor akt/mtor pathway endothelial cell dysfunction renin-angiotensin system inhibitor oxidative stress apoptosis endothelial cell dysfunction Medicine R
spellingShingle	apoptosis oxidative stress renin-angiotensin system inhibitor akt/mtor pathway endothelial cell dysfunction renin-angiotensin system inhibitor oxidative stress apoptosis endothelial cell dysfunction Medicine R Xuekun Shi Yuhua Guan Shaoyan Jiang Tiandong Li Bing Sun Huan Cheng Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway
description	Introduction The renin-angiotensin system is associated with blood pressure regulation, inflammation, oxidative stress and insulin resistance. It can decrease intracellular oxidative stress. Stimulation with H 2 O 2 leads to increased oxidative stress and activation of the AKT/mTOR pathway. However, the role of renin-angiotensin system inhibitors in oxidative stress-induced endothelial cell dysfunction and H 2 O 2 -induced AKT activation remains unclear. Material and methods Human coronary artery endothelial cells (HCAECs) were used. The cells were treated with H 2 O 2 , captopril, the AKT inhibitor MK-2206, and the AKT activator SC79, either separately, or in combination. p53 and ICAM-1 expression, and p-eNOS, p-Akt and mTOR activation were measured by Western blot. Cell viability was assessed by MTT assay. Levels of reactive oxygen species (ROS) were assayed by flow cytometry. Proliferation was monitored by BrdU labeling, while cell migration and invasion were determined by wound healing and Transwell assays, respectively. Results The renin-angiotensin system inhibitor captopril reversed H 2 O 2 -induced oxidative stress and apoptosis in HCAECs. Co-treatment with captopril and the AKT inhibitor MK-2206 reduced the H 2 O 2 -induced P53 and ICAM-1 protein expression (p < 0.05). The proliferation, migration and invasion of HCAECs were significantly enhanced by co-treatment with captopril and MK-2206 (p < 0.05). Conclusions The study revealed the protective effect of captopril against H 2 O 2 -induced endothelial cell dysfunction through the AKT/mTOR pathway, and its enhancement of cell survival. These findings provide new insights into the protective effects of captopril and novel therapeutic approaches to treatment of cardiovascular disease.
format	article
author	Xuekun Shi Yuhua Guan Shaoyan Jiang Tiandong Li Bing Sun Huan Cheng
author_facet	Xuekun Shi Yuhua Guan Shaoyan Jiang Tiandong Li Bing Sun Huan Cheng
author_sort	Xuekun Shi
title	Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway
title_short	Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway
title_full	Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway
title_fullStr	Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway
title_full_unstemmed	Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway
title_sort	renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the pi3k/akt/mtor pathway
publisher	Termedia Publishing House
publishDate	2018
url	https://doaj.org/article/41de30315c8f433fa7c4c5fcc3ec009c
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Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway

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