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
Stimulation of adenosine A(2B) receptors induces interleukin-6 secretion in cardiac fibroblasts via the PKC-delta-P38 signalling pathway
Feng, Wei; Song, Yao; Chen, Chao; Lu, Zhi Zhen; Zhang, Youyi1
关键词a(2b) Adenosine Receptors Cardiac Fibroblasts Il-6 Pkc Delta
刊名BRITISH JOURNAL OF PHARMACOLOGY
2010-04-01
DOI10.1111/j.1476-5381.2009.00558.x
159期:8页:1598-1607
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy
研究领域[WOS]Pharmacology & Pharmacy
关键词[WOS]PROTEIN-KINASE-C ; CONGESTIVE-HEART-FAILURE ; PROINFLAMMATORY CYTOKINES ; IL-6 EXPRESSION ; P38 MAPK ; CELLS ; ACTIVATION ; INHIBITION ; INCREASE ; PKC
英文摘要

Background and purpose:

Inflammatory response and cytokine activation are markedly stimulated after myocardial infarction, and contribute to cardiac remodelling. Interleukin-6 (IL-6), a pro-inflammatory cytokine, has pleiotropic effects on cardiac remodelling. Adenosine, released by all cell types, binds to a class of G protein-coupled receptors to induce various cardiovascular effects. The aim of this work was to investigate whether activation of adenosine receptors, particularly A(2B) adenosine receptors, could stimulate IL-6 secretion in cardiac fibroblasts (CFs).

Experimental approach:

elisa was used to assess IL-6 concentration in supernatant, and immunostaining was used to analyse IL-6 protein level in CFs. The levels of phosphorylated and total p38, extracellular signal-regulated kinase, c-Jun N-terminal kinase and protein kinase C-delta (PKC-delta) were determined by Western blot analysis.

Key results:

Adenosine-5′-N-ethyluronamide (NECA), a stable adenosine analogue, dose- and time-dependently stimulated IL-6 secretion in CFs. The effect of NECA was dose-dependently inhibited by an A(2B) antagonist, and silencing of the A(2B) receptor also inhibited IL-6 secretion. By using PKC isoform-selective inhibitors and translocation peptide inhibitors, the PKC-delta isoform was found to be involved in the up-regulation of IL-6 production. Inhibition of p38 by SB203580, and adenoviral transfer of dominant-negative p38 inhibited NECA-induced IL-6 production. Furthermore, PKC-delta functioned as an upstream regulator of p38 MAPK in this process.

Conclusions and implications:

We demonstrated a novel relationship between adenosine and IL-6 secretion, in that IL-6 secretion induced by NECA was mediated by adenosine A(2B) receptor activation in CFs and was dependent on a PKC delta-P38 pathway.

This article is commented on by Cohen et al., pp. 1595-1597 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476-5381.2010.00668.x.

语种英语
WOS记录号WOS:000276127000006
Citation statistics
Cited Times:28[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/400002259/57312
Collection北京大学第三临床医学院_心血管内科
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China
2.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100191, Peoples R China
Recommended Citation
GB/T 7714
Feng, Wei,Song, Yao,Chen, Chao,et al. Stimulation of adenosine A(2B) receptors induces interleukin-6 secretion in cardiac fibroblasts via the PKC-delta-P38 signalling pathway[J]. BRITISH JOURNAL OF PHARMACOLOGY,2010,159(8):1598-1607.
APA Feng, Wei,Song, Yao,Chen, Chao,Lu, Zhi Zhen,&Zhang, Youyi.(2010).Stimulation of adenosine A(2B) receptors induces interleukin-6 secretion in cardiac fibroblasts via the PKC-delta-P38 signalling pathway.BRITISH JOURNAL OF PHARMACOLOGY,159(8),1598-1607.
MLA Feng, Wei,et al."Stimulation of adenosine A(2B) receptors induces interleukin-6 secretion in cardiac fibroblasts via the PKC-delta-P38 signalling pathway".BRITISH JOURNAL OF PHARMACOLOGY 159.8(2010):1598-1607.
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