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Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats.
Exp Physiol. 2019 06; 104(6):946-956.EP

Abstract

NEW FINDINGS

What is the central question of this study? Is the membrane raft redox signalling pathway involved in blood pressure increase, endothelial dysfunction and vascular remodelling in an angiotensin II-induced hypertensive animal model? What is the main finding and its importance? The membrane raft redox signalling pathway was involved in endothelial dysfunction and medial remodelling in angiotensin II-induced hypertension.

ABSTRACT

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 Sprague-Dawley 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 α 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.

Authors+Show Affiliations

Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China. Laboratory of Vascular Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Shanghai Institute of Hypertension, Shanghai, China. Laboratory of Vascular Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30924217

Citation

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, vol. 104, no. 6, 2019, pp. 946-956.
Wei J, Xu L, Du YN, et al. Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats. Exp Physiol. 2019;104(6):946-956.
Wei, J., Xu, L., Du, Y. N., Tang, X. F., Ye, M. Q., Wu, Y. J., Han, W. Q., & Gao, P. J. (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. https://doi.org/10.1113/EP087335
Wei J, et al. Membrane Raft Redox Signalling Contributes to Endothelial Dysfunction and Vascular Remodelling of Thoracic Aorta in Angiotensin II-infused Rats. Exp Physiol. 2019;104(6):946-956. PubMed PMID: 30924217.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II-infused rats. AU - Wei,Jian, AU - Xu,Lian, AU - Du,Ya-Nan, AU - Tang,Xiao-Feng, AU - Ye,Mao-Qing, AU - Wu,Yong-Jie, AU - Han,Wei-Qing, AU - Gao,Ping-Jin, Y1 - 2019/05/01/ PY - 2018/08/27/received PY - 2019/03/12/accepted PY - 2019/3/30/pubmed PY - 2020/7/25/medline PY - 2019/3/30/entrez KW - angiotensin II KW - endothelial dysfunction KW - hypertension KW - membrane rafts KW - vascular remodelling SP - 946 EP - 956 JF - Experimental physiology JO - Exp Physiol VL - 104 IS - 6 N2 - NEW FINDINGS: What is the central question of this study? Is the membrane raft redox signalling pathway involved in blood pressure increase, endothelial dysfunction and vascular remodelling in an angiotensin II-induced hypertensive animal model? What is the main finding and its importance? The membrane raft redox signalling pathway was involved in endothelial dysfunction and medial remodelling in angiotensin II-induced hypertension. ABSTRACT: 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 Sprague-Dawley 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 α 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. SN - 1469-445X UR - https://www.unboundmedicine.com/medline/citation/30924217/Membrane_raft_redox_signalling_contributes_to_endothelial_dysfunction_and_vascular_remodelling_of_thoracic_aorta_in_angiotensin_II_infused_rats_ L2 - https://doi.org/10.1113/EP087335 DB - PRIME DP - Unbound Medicine ER -