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学科主题: 临床医学
题名:
Stimulation of adenosine A(2B) receptors induces interleukin-6 secretion in cardiac fibroblasts via the PKC-delta-P38 signalling pathway
作者: 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
发表日期: 2010-04-01
DOI: 10.1111/j.1476-5381.2009.00558.x
卷: 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
所属项目编号: 2006CB503806 ; 30570716 ; 30821001 ; 307001
项目资助者: National Key Basic Research Program of the People&prime ; s Republic of China ; Natural Science Foundation of China ; Key Grant Project of Chinese Ministry of Education
WOS记录号: WOS:000276127000006
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57312
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.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:
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.
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