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学科主题: 临床医学
题名:
Cortistatin attenuates vascular calcification in rats
作者: Liu, Yue1; Zhou, Ye Bo2; Zhang, Gai Gai1; Cai, Yan2; Duan, Xiao Hui2; Teng, Xu2; Song, Jun Qiu2; Shi, Yi2; Tang, Chao Shu2,3,4; Yin, Xin Hua1; Qi, Yong Fen2,3,4
关键词: Cortistatin ; Vascular calcification ; Receptor ; Rat
刊名: REGULATORY PEPTIDES
发表日期: 2010-01-08
DOI: 10.1016/j.regpep.2009.09.005
卷: 159, 期:1-3, 页:35-43
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism ; Physiology
研究领域[WOS]: Endocrinology & Metabolism ; Physiology
关键词[WOS]: SMOOTH-MUSCLE-CELLS ; SOMATOSTATIN RECEPTORS ; IN-VITRO ; DISEASE ; NEUROPEPTIDE ; MECHANISMS ; EXPRESSION ; RESPONSES ; NICOTINE ; GHRELIN
英文摘要:

Cortistatin (CST) is a newly discovered polypeptide with multiple biological activities that plays a regulatory role in the nervous, endocrine and immune systems. However, the role of CST in the pathogenesis of cardiovascular diseases remains unclear. In this study, we investigated in rats whether CST inhibits vascular calcification induced by vitamin D3 and nicotine treatment in vivo and calcification of cultured rat vascular smooth muscular cells (VSMCs) induced by beta-glycerophosphate in vitro and the underlying mechanism. We measured rat hemodynamic variables, alkaline phosphatase (ALP) activity, calcium deposition and pathological changes in aortic tissues and cultured VSMCs. CST treatment significantly improved hemodynamic values and arterial compliance in rats with vascular calcification by decreasing systolic, blood pressure, pulse pressure, left ventricular end-systolic pressure and left ventricular end-diastolic pressure. CST also significantly decreased ALP activity and calcium deposition, alleviated pathological injury and down-regulated the mRNA expression of type III sodium-dependent phosphate co-transporter-1 (Pit-1) in aortic tissues. It dose-independently inhibited the calcification of VSMCs by decreasing ALP activity and calcium deposition, alleviating pathologic injury and down-regulating Pit-1 mRNA expression. As with CST treatment, ALP activation and calcium deposition were decreased significantly on treatment with ghrelin, the endogenous agonist of growth hormone secretagogue receptor 1a (CHSR1a), but not significantly with somatostatin-14 or proadrenomedullin N-terminal 20 peptide in VSMCs. Further, growth hormone-releasing peptide-6[D-lys], the endogenous antagonist of GHSR1a, markedly reversed the increased ALP activity and calcium deposition in VSMCs. CST could be a new target molecule for the prevention and therapy of vascular calcification, whose effects are mediated by GHSR1a rather than SSTRs or Mrg X2. (C) 2009 Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: 2006CB503807 ; 30670847 ; 30871013 ; 30470693
项目资助者: Major Basic Research Program of China ; National Natural Science Foundation of China
WOS记录号: WOS:000273920500007
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66853
Appears in Collections:北京大学第一临床医学院_心血管内科_期刊论文

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作者单位: 1.Harbin Med Univ, Affiliated Hosp 1, Dept Cardiol, Harbin 150086, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
3.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
4.Peking Univ, Hosp 1, Inst Cardiovasc Dis, Beijing 100034, Peoples R China

Recommended Citation:
Liu, Yue,Zhou, Ye Bo,Zhang, Gai Gai,et al. Cortistatin attenuates vascular calcification in rats[J]. REGULATORY PEPTIDES,2010,159(1-3):35-43.
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