Sulforaphane Attenuates Angiotensin II-Induced Vascular Smooth Muscle Cell Migration via Suppression of NOX4/ROS/Nrf2 Signaling

被引:30
作者
Zhang, Min [1 ]
Xu, Yingjie [1 ]
Qiu, Zhaohui [1 ]
Jiang, Li [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, TongRen Hosp, Div Cardiol, 1111 Xianxia Rd, Shanghai 200336, Peoples R China
关键词
sulforaphane; angiotensin II; human vascular smooth muscle cells; nuclear respiratory factor 2; reactive oxygen species; UP-REGULATION; ENDOTHELIAL-CELLS; OXIDATIVE STRESS; KAPPA-B; PROLIFERATION; ACTIVATION; ANGIOGENESIS; DYSFUNCTION; INHIBITION; EXPRESSION;
D O I
10.7150/ijbs.28874
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Angiotensin II (Ang II) is involved in the pathogenic progress of cardiovascular diseases via the promotion of abnormal proliferation and migration of human vascular smooth muscle cells (HVSMCs). Sulforaphane (SFN) exerts potent anti-inflammatory effects both in vitro and in vivo. In the present study, we aimed to investigate the effects of SFN on Ang II-induced abnormal migration of HVSMCs as well as the underlying mechanisms of those effects. The results showed that Ang II-induced HVSMC proliferation and migration were inhibited by treatment with SFN. SFN also exhibited anti-inflammatory activity, as indicated by its reduction of monocyte adhesion to HVSMCs via the reduction of ICAM1 and VCAM1 levels. Moreover, SFN reduced the Ang II-induced upregulation of HVSMC migration; this effect was inhibited by pretreatment with inhibitors of NADPH oxidase and ROS or transfection with siNOX4. In addition, SFN reversed the Ang II-induced upregulation of HVSMC migration via elevation of Nrf2 activation and expression. Taken together, the results indicate that SFN reverses Ang II-induced HVSMC migration through suppression of the NOX4/ROS/Nrf2 pathway. Thus, SFN is a potential agent to reverse the pathological changes involved in various cardiovascular diseases.
引用
收藏
页码:148 / 157
页数:10
相关论文
共 32 条
[1]   Endothelial Microparticles From Acute Coronary Syndrome Patients Induce Premature Coronary Artery Endothelial Cell Aging and Thrombogenicity Role of the Ang II/AT1 Receptor/NADPH Oxidase-Mediated Activation of MAPKs and PI3-Kinase Pathways [J].
Abbas, Malak ;
Jesel, Laurence ;
Auger, Cyril ;
Amoura, Lamia ;
Messas, Nathan ;
Manin, Guillaume ;
Rumig, Cordula ;
Leon-Gonzalez, Antonio J. ;
Ribeiro, Thais P. ;
Silva, Grazielle C. ;
Abou-Merhi, Raghida ;
Hamade, Eva ;
Hecker, Markus ;
Georg, Yannick ;
Chakfe, Nabil ;
Ohlmann, Patrick ;
Schini-Kerth, Valerie B. ;
Toti, Florence ;
Morel, Olivier .
CIRCULATION, 2017, 135 (03) :280-+
[2]  
Adachi Sen, 2016, J Clin Med Res, V8, P743, DOI 10.14740/jocmr2675w
[3]   Nrf2/Keap1 system regulates vascular smooth muscle cell apoptosis for vascular homeostasis: role in neointimal formation after vascular injury [J].
Ashino, Takashi ;
Yamamoto, Masayuki ;
Numazawa, Satoshi .
SCIENTIFIC REPORTS, 2016, 6
[4]   Redox-Sensitive Transcription Factor Nrf2 Regulates Vascular Smooth Muscle Cell Migration and Neointimal Hyperplasia [J].
Ashino, Takashi ;
Yamamoto, Masayuki ;
Yoshida, Takemi ;
Numazawa, Satoshi .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2013, 33 (04) :760-U273
[5]   Epigallocatechin-3-gallate promotes angiogenesis via up-regulation of Nfr2 signaling pathway in a mouse model of ischemic stroke [J].
Bai, Qian ;
Lyu, Zhipai ;
Yang, Xianhui ;
Pang, Zhenjie ;
Lou, Jiyu ;
Dong, Tieli .
BEHAVIOURAL BRAIN RESEARCH, 2017, 321 :79-86
[6]   Angiotensin II stimulates matrix metalloproteinase secretion in human vascular smooth muscle cells via nuclear factor-κB and activator protein 1 in a redox-sensitive manner [J].
Browatzki, M ;
Larsen, D ;
Pfeiffer, CAH ;
Gehrke, SG ;
Schmidt, J ;
Kranzhöfer, A ;
Katus, HA ;
Kranzhöfer, R .
JOURNAL OF VASCULAR RESEARCH, 2005, 42 (05) :415-423
[7]   Expression of Human Tissue Factor Pathway Inhibitor on Vascular Smooth Muscle Cells Inhibits Secretion of Macrophage Migration Inhibitory Factor and Attenuates Atherosclerosis in ApoE-/- Mice [J].
Chen, Daxin ;
Xia, Min ;
Hayford, Claudia ;
Tham, El-Li ;
Semik, Vikki ;
Hurst, Stuart ;
Chen, Ying ;
Tam, Henry H. ;
Pan, Jun ;
Wang, Yucheng ;
Tan, Xiaojin ;
Lan, Hui-Yao ;
Shen, Huahao ;
Kakkar, Vijay V. ;
Xu, Qingbo ;
McVey, John H. ;
Dorling, Anthony .
CIRCULATION, 2015, 131 (15) :1350-U101
[8]   Loss of Smooth Muscle α-Actin Leads to NF-κB-Dependent Increased Sensitivity to Angiotensin II in Smooth Muscle Cells and Aortic Enlargement [J].
Chen, Jiyuan ;
Peters, Andrew ;
Papke, Christina L. ;
Villamizar, Carlos ;
Ringuette, Lea-Jeanne ;
Cao, Jiumei ;
Wang, Shanzhi ;
Ma, Shuangtao ;
Gong, Limin ;
Byanova, Katerina L. ;
Xiong, Jian ;
Zhu, Michael X. ;
Madonna, Rosalinda ;
Kee, Patrick ;
Geng, Yong-Jian ;
Brasier, Allan R. ;
Davis, Elaine C. ;
Prakash, Siddharth ;
Kwartler, Callie S. ;
Milewicz, Dianna M. .
CIRCULATION RESEARCH, 2017, 120 (12) :1903-+
[9]   LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and EpithelialMesenchymal Transition [J].
Chen, Yi ;
Peng, Ya ;
Xu, Zhipeng ;
Ge, Bo ;
Xiang, Xuebao ;
Zhang, Tianyu ;
Gao, Li ;
Shi, Hailin ;
Wang, Chuang ;
Huang, Jiefu .
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2017, 41 (06) :2399-2410
[10]   Dipeptidyl peptidase-4 inhibition by gemigliptin prevents abnormal vascular remodeling via NF-E2-related factor 2 activation [J].
Choi, Seung Hee ;
Park, Sungmi ;
Oh, Chang Joo ;
Leem, Jaechan ;
Park, Keun-Gyu ;
Lee, In-Kyu .
VASCULAR PHARMACOLOGY, 2015, 73 :11-19