Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone acetate-salt hypertensive mice

被引:16
|
作者
Sheng, Li-Juan [1 ,2 ]
Ruan, Cheng-Chao [1 ,2 ,3 ,4 ,5 ]
Ma, Yu [1 ,2 ]
Chen, Dong-Rui [1 ,2 ]
Kong, Ling-Ran [1 ,2 ]
Zhu, Ding-Liang [1 ,2 ]
Gao, Ping-Jin [1 ,2 ,3 ,4 ,5 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp,Shanghai Inst Hypertens, State Key Lab Med Gen,Shanghai Key Lab Hypertens, Shanghai 200025, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Hypertens, Dept Hypertens,Ruijin Hosp, Shanghai 200025, Peoples R China
[3] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Vasc Biol, Shanghai, Peoples R China
[4] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China
[5] Shanghai Jiao Tong Univ, Sch Med, Shanghai 200025, Peoples R China
基金
中国国家自然科学基金;
关键词
beta3 adrenergic receptor; DOCA-salt hypertensive mice; hypertension; let-7b; perivascular adipose tissue; vascular injury; PERIVASCULAR ADIPOSE-TISSUE; BETA-3-ADRENERGIC RECEPTOR; DISEASE; BETA(3)-ADRENOCEPTORS; ADIPOCYTES; ACTIVATION; MOUSE;
D O I
10.1002/1873-3468.12107
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
Beta3 adrenergic receptor (ADRB3) mediates vessel relaxation in the endothelium while it modulates lipolysis in the adipose tissue. However, the function and regulation mechanism of ADRB3 in the perivascular adipose tissue (PVAT), especially in hypertension, is still unclear. We show that ADRB3 protein is upregulated in the PVAT of deoxycorticosterone acetate-salt (DOCA-salt) hypertensive mice, with the characteristics of PVAT browning and increased uncoupling protein 1 (UCP1) expression. Inhibition of ADRB3 with selective antagonist SR59230A caused serious vascular injury in vivo, even though UCP1 expression was downregulated. ADRB3 protein was regulated by let-7b, which was decreased in the PVAT of the DOCA-salt group. These data reveal that ADRB3 in PVAT contributes to vascular function in the progression of hypertension.
引用
收藏
页码:769 / 778
页数:10
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