Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway
机构：[a]Department of Cardiovascular Medicine, Shenzhen Longhua District Central Hospital, Longhua Central Hospital Affiliated Guangdong Medical University, Shenzhen, Guangdong Province 518110, China[b]Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China[c]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, and Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing 100029, China临床科室急诊危重症中心首都医科大学附属安贞医院[d]Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan 430060, China
Background: Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms. Methods: Sesn2 expression was detected in aortas collected from AD patients and normal donors. In addition, blood samples were collected from AD patients and non-AD (NAD) patients, and the plasma Sesn2 levels were measured. Furthermore, the effects of Sesn2 on angiotensin (Ang) II-induced smooth muscle cell (SMC) apoptosis were investigated in vitro. Results: Compared with the aortas from normal donors, aortas from AD patients had significantly increased Sesn2. Sesn2 was mainly secreted by macrophages, and low levels were secreted by CD4+ T lymphocytes, but not SMCs. Plasma Sesn2 levels were also increased in AD patients compared with NAD patients. Sesn2 levels were negatively corrected with superoxide dismutase (SOD) levels but positively corrected with mal-ondialdehyde (MDA) levels in AD patients. In co-cultures of macrophages and SMCs, Sesn2 overexpression in macrophages significantly reduced Ang II-induced SMC apoptosis, and this effect could be reversed by Nrf2 silencing. Conclusions: Sesn2 is increased in both aortas and plasma from AD patients. Sesn2 may alleviate Ang II-induced SMC apoptosis and participate in AD via the Nrf2 pathway. Sesn2 may be a new target in the treatment and prevention of AD.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81770472, 81460081, 81460061, 81760051]
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2018]版：
大类|3 区医学
小类|3 区医学：研究与实验3 区药学
最新[2023]版：
大类|2 区医学
小类|2 区医学：研究与实验2 区药学
JCR分区：
出版当年[2017]版：
Q2PHARMACOLOGY & PHARMACYQ2MEDICINE, RESEARCH & EXPERIMENTAL
最新[2023]版：
Q1MEDICINE, RESEARCH & EXPERIMENTALQ1PHARMACOLOGY & PHARMACY
第一作者机构：[a]Department of Cardiovascular Medicine, Shenzhen Longhua District Central Hospital, Longhua Central Hospital Affiliated Guangdong Medical University, Shenzhen, Guangdong Province 518110, China
共同第一作者：
通讯作者：
通讯机构：[a]Department of Cardiovascular Medicine, Shenzhen Longhua District Central Hospital, Longhua Central Hospital Affiliated Guangdong Medical University, Shenzhen, Guangdong Province 518110, China[b]Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China
推荐引用方式(GB/T 7714)：
Ting Xiao,Le Zhang,Ying Huang,et al.Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway[J].LIFE SCIENCES.2019,218:132-138.doi:10.1016/j.lfs.2018.12.043.
APA：
Ting Xiao,Le Zhang,Ying Huang,Ying Shi,Jing Wang...&Hongtao Liu.(2019).Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway.LIFE SCIENCES,218,
MLA：
Ting Xiao,et al."Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway".LIFE SCIENCES 218.(2019):132-138
医学