IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科
学科主题临床医学
Endogenous calcitonin gene-related peptide protects human alveolar epithelial cells through protein kinase C epsilon and heat shock protein
Wang, W; Jia, LY; Wang, TK; Sun, WT; Wu, S; Wang, X
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2005-05-27
DOI10.1074/jbc.M413864200
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
Cited Times:24[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67652
Collection北京大学第三临床医学院_心血管内科
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
GB/T 7714
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.
APA Wang, W,Jia, LY,Wang, TK,Sun, WT,Wu, S,&Wang, X.(2005).Endogenous calcitonin gene-related peptide protects human alveolar epithelial cells through protein kinase C epsilon and heat shock protein.JOURNAL OF BIOLOGICAL CHEMISTRY,280(21),20325-20330.
MLA Wang, W,et al."Endogenous calcitonin gene-related peptide protects human alveolar epithelial cells through protein kinase C epsilon and heat shock protein".JOURNAL OF BIOLOGICAL CHEMISTRY 280.21(2005):20325-20330.
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