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论文题目: Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone acetate-salt hypertensive mice
英文论文题目: Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone acetate-salt hypertensive mice
第一作者: Sheng, LJ; Ruan, CC; Ma, Y; Chen, DR; Kong, LR; Zhu, DL; Gao, PJ
英文第一作者: Sheng, LJ; Ruan, CC; Ma, Y; Chen, DR; Kong, LR; Zhu, DL; Gao, PJ
联系作者: Ruan, CC (reprint author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Hypertens, Ruijin Hosp, 197 Ruijin 2nd Rd, Shanghai 200025, Peoples R China.
英文联系作者: Ruan, CC (reprint author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Hypertens, Ruijin Hosp, 197 Ruijin 2nd Rd, Shanghai 200025, Peoples R China.
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发表年度: 2016
卷: 590
期: 6
页码: 769-778
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.
英文摘要: 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.
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学科: Biochemistry & Molecular Biology; Biophysics; Cell Biology
英文学科: Biochemistry & Molecular Biology; Biophysics; Cell Biology
影响因子: 3.623
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论文类别: Article
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