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学科主题: 基础医学
题名:
Intermedin(1-53) attenuates vascular smooth muscle cell calcification by inhibiting endoplasmic reticulum stress via cyclic adenosine monophosphate/protein kinase A pathway
作者: Zhu, Yi1,2; Chang, Jin-Rui1,2; Duan, Xiao-Hui2; Zhang, Bao-Hong3; Teng, Xu2; Zhou, Ye-Bo2; Liu, Yue4; Yu, Yan-Rong5; Tang, Chao-Shu1,2; Qi, Yong-Fen2,5
关键词: intermedin(1-53) ; vascular calcification ; endoplasmic reticulum stress ; apoptosis
刊名: EXPERIMENTAL BIOLOGY AND MEDICINE
发表日期: 2013-10-01
DOI: 10.1177/1535370213502619
卷: 238, 期:10, 页:1136-1146
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Medicine, Research & Experimental
研究领域[WOS]: Research & Experimental Medicine
关键词[WOS]: SIGNALING PATHWAY ; ADRENOMEDULLIN ; APOPTOSIS ; PEPTIDE ; PROTEIN ; INJURY ; MECHANISMS ; RECEPTOR ; RATS
英文摘要:

We previously reported that endoplasmic reticulum (ER) stress-mediated apoptosis participated in vascular calcification. Importantly, a novel paracrine/autocrine peptide intermedin(1-53) (IMD1-53) in the vasculature inhibited vascular calcification in rats. But the mechanisms needed to be fully elucidated. Vascular smooth muscle cells (VSMCs) calcification was induced by CaCl2 and beta-glycerophosphate. Tunicamycin (Tm) or dithiothreitol (DTT) was used to induce ER stress. We found that IMD1-53 (10(-7) mol/L) treatment significantly alleviated the protein expression of ER stress hallmarks activating transcription factor 4 (ATF4), ATF6, glucose-regulated protein 78 (GRP78) and GRP94 induced by Tm or DTT. ER stress occurred in early and late calcification of VSMCs but was inhibited by IMD1-53. These inhibitory effects of IMD1-53 were abolished by treatment with the protein kinase A (PKA) inhibitor H89. Pretreatment with IMD1-53 decreased the number of apoptotic VSMCs and downregulated protein expression of cleaved caspase 12 and C/EBP homologous protein (CHOP) in calcified VSMCs. Concurrently, IMD1-53 restored the loss of VSMC lineage markers and ameliorated calcium deposition and alkaline phosphatase activity in calcified VSMCs as well. The observation was further verified by Alizarin Red S staining, which showed that IMD1-53 reduced positive red nodules among calcified VSMCs. In conclusion, IMD1-53 attenuated VSMC calcification by inhibiting ER stress through cAMP/PKA signalling.

语种: 英语
所属项目编号: 81270407 ; 81170082 ; 81100229 ; 20110001110012
项目资助者: National Natural Science Foundation of China ; Ministry of Education Foundation for Doctoral Tutor ; Leading Academic Discipline Project of Beijing Education Bureau
WOS记录号: WOS:000324914200006
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50274
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Sch Basic Med Sci, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Key Lab Mol Cardiovasc Sci, Minist Educ, Beijing 100191, Peoples R China
3.Capital Inst Pediat, Beijing 100020, Peoples R China
4.Harbin Med Univ, Dept Cardiol, Affiliated Hosp 1, Harbin 150001, Peoples R China
5.Peking Univ, Lab Cardiovasc Bioact Mol, Sch Basic Med Sci, Beijing 100191, Peoples R China

Recommended Citation:
Zhu, Yi,Chang, Jin-Rui,Duan, Xiao-Hui,et al. Intermedin(1-53) attenuates vascular smooth muscle cell calcification by inhibiting endoplasmic reticulum stress via cyclic adenosine monophosphate/protein kinase A pathway[J]. EXPERIMENTAL BIOLOGY AND MEDICINE,2013,238(10):1136-1146.
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