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学科主题: 临床医学
题名:
Endogenous calcitonin gene-related peptide protects human alveolar epithelial cells through protein kinase C epsilon and heat shock protein
作者: Wang, W; Jia, LY; Wang, TK; Sun, WT; Wu, S; Wang, X
刊名: JOURNAL OF BIOLOGICAL CHEMISTRY
发表日期: 2005-05-27
DOI: 10.1074/jbc.M413864200
卷: 280, 期:21, 页:20325-20330
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology
研究领域[WOS]: Biochemistry & Molecular Biology
关键词[WOS]: MYOCARDIAL-INFARCTION ; NITRIC-OXIDE ; INJURY ; REPERFUSION ; MODULATION ; PHYSIOLOGY ; CGRP ; PKC ; ACTIVATION ; RECEPTORS
英文摘要:

The intracellular mechanisms of ischemic preconditioning (PC) in preventing lung dysfunction following transplantation, shock, and trauma remain poorly understood. Previously, we have shown that alveolar epithelial cells secrete calcitonin gene-related peptide (CGRP) under inflammatory stress. Using a hypoxia/reoxygenation (H/R) and PC model, we found that CGRP was also secreted from human type II alveolar epithelial cells (A549) after PC. The locally released CGRP interacted with its receptor on the membrane of A549 cells and elicited downstream signals mediating the PC effect, because hCGRP(8-37), a specific CGRP receptor antagonist, attenuated the protective effect of PC. Preinhibition of CGRP protein synthesis by small interfering RNA exacerbated (but overexpression of the CGRP gene ameliorated) H/R-induced cell death, which supports the autocrine effect of CGRP on A549 cells. Exogenous bioactive CGRP mimicked the beneficial effect of PC and up-regulated the expression of heat shock protein 70 (HSP70), which might act as the end effector to maintain cell viability. These effects were sensitive to hCGRP(8-37), calphostin C (a protein kinase C (PKC) inhibitor), and 5-hydroxydecanoic acid ( a mitochondrial K-ATP(+) channel blocker) but were insensitive to protein kinase A blockers. Moreover, CGRP induced the membrane translocation of PKC is an element of. PKCV1-2 (a cell-permeable inhibitory peptide of PKC is an element of) effectively abolished CGRP-induced HSP70 expression and cell protection. Therefore, PC induces CGRP secretion from human alveolar epithelial cells, and the locally released CGRP acts back on these cells, protecting them from H/R injury. The post-receptor signaling of CGRP is through PKC is an element of-dependent expression of HSP70.

语种: 英语
WOS记录号: WOS:000229242000022
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67652
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100083, Peoples R China
2.Peking Univ, Dept Physiol, Key Lab Mol Cardiovasc Sci, Minist Educ,Hlth Sci Ctr, Beijing 100083, Peoples R China

Recommended Citation:
Wang, W,Jia, LY,Wang, TK,et al. Endogenous calcitonin gene-related peptide protects human alveolar epithelial cells through protein kinase C epsilon and heat shock protein[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2005,280(21):20325-20330.
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