Sheng Li-Juan, Ruan Cheng-Chao, Ma Yu, Chen Dong-Rui, Kong Ling-Ran, Zhu Ding-Liang, Gao Ping-Jin
State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension and Department of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Laboratory of Vascular Biology and Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China.
FEBS Lett. 2016 Mar;590(6):769-78. doi: 10.1002/1873-3468.12107. Epub 2016 Mar 3.
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.
β3肾上腺素能受体（ADRB3）在内皮中介导血管舒张，同时在脂肪组织中调节脂肪分解。然而，ADRB3在血管周围脂肪组织（PVAT）中的功能和调控机制，尤其是在高血压中的情况，仍不清楚。我们发现，在醋酸脱氧皮质酮-盐（DOCA-盐）高血压小鼠的PVAT中，ADRB3蛋白上调，具有PVAT褐变和解偶联蛋白1（UCP1）表达增加的特征。用选择性拮抗剂SR59230A抑制ADRB3在体内会导致严重的血管损伤，尽管UCP1表达下调。ADRB3蛋白受let-7b调控，在DOCA-盐组的PVAT中let-7b减少。这些数据表明，PVAT中的ADRB3在高血压进展过程中对血管功能有贡献。
