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Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats

文献类型：期刊论文

作者Wei, Jian1,2; Xu, Lian1,2; Du, Ya-Nan1,2; Tang, Xiao-Feng1,2; Ye, Mao-Qing1,2; Wu, Yong-Jie1,2; Han, Wei-Qing1,2; Gao, Ping-Jin1,2,3; Han, Wei-Qing3; ,
刊名EXPERIMENTAL PHYSIOLOGY
出版日期2019
卷号104期号:6页码:946-956
关键词angiotensin II endothelial dysfunction hypertension membrane rafts vascular remodelling
ISSN号0958-0670
DOI10.1113/EP087335
文献子类Article
英文摘要The membrane raft (MR) redox pathway is characterized by NADPH oxidase activation via the clustering of its subunits through lysosome fusion and the activation of acid sphingomyelinase (ASMase). Our previous study shows that the MR redox signalling pathway is associated with angiontensin II (AngII)-induced production of reactive oxygen species (ROS) and endothelial dysfunction in rat mesenteric arteries. In the present study, we hypothesized that this signalling pathway is involved in blood pressure increase, endothelial dysfunction and vascular remodelling in an AngII-induced hypertensive animal model. Sixteen-week-old male SpragueDawley rats were subjected to AngII infusion for 2 weeks with or without treatment with the lysosome fusion inhibitor bafilomycin A1 and ASMase inhibitor amitriptyline. After treatments, aortas were harvested for further study. The results showed that the MR redox signalling pathway was activated as indicated by the increase of MR formation, ASMase activity and ROS production in aorta from AngII-infused rats compared with that from control rats. MR formation and ROS production were significantly inhibited in thoracic aorta from AngII-induced rats treated with bafilomycin A1 and amitriptyline. Both treatments significantly attenuated blood pressure increase, endothelial dysfunction and vascular remodelling including medial hypertrophy, and increased collagen and fibronectin deposition in thoracic aortas from AngII-infused rats. Finally, both treatments significantly prevented the increase of inflammatory factors including monocyte chemotactic protein 1, intercellular adhesion molecule 1 and tumour necrosis factor a in thoracic aorta from AngII-infused rats. In conclusion, the present study demonstrates that the MR redox signalling pathway was involved in endothelial dysfunction and medial remodelling in AngII-induced hypertension.
学科主题Physiology
WOS关键词NADPH OXIDASE ACTIVATION ; H+-ATPASE ACTIVITY ; OXIDATIVE STRESS ; ACID SPHINGOMYELINASE ; LYSOSOME FUSION ; LIPID RAFTS ; INTERCALATED CELLS ; NAD(P)H OXIDASE ; BLOOD-PRESSURE ; AMITRIPTYLINE
语种英语
WOS记录号WOS:000483740300018
出版者WILEY
版本出版稿
源URL[http://202.127.25.144/handle/331004/564]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Key Lab Hypertens, 197 Ruijin 2nd Rd, Shanghai 200025, Peoples R China;
2.Shanghai Res Inst Hypertens, Shanghai, Peoples R China;
3.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Vasc Biol, Shanghai, Peoples R China,
推荐引用方式
GB/T 7714		 Wei, Jian,Xu, Lian,Du, Ya-Nan,et al. Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats[J]. EXPERIMENTAL PHYSIOLOGY,2019,104(6):946-956.
APA Wei, Jian.,Xu, Lian.,Du, Ya-Nan.,Tang, Xiao-Feng.,Ye, Mao-Qing.,...&,.(2019).Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats.EXPERIMENTAL PHYSIOLOGY,104(6),946-956.
MLA Wei, Jian,et al."Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats".EXPERIMENTAL PHYSIOLOGY 104.6(2019):946-956.

入库方式： OAI收割

来源：上海营养与健康研究所

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