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IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科  > 期刊论文
学科主题: 临床医学
题名:
Interleukin-6 family of cytokines mediates isoproterenol-induced delayed STAT3 activation in mouse heart
作者: Yin, F1; Li, P1; Zheng, M1; Chen, L1; Xu, Q1; Chen, K1; Wang, YY1; Zhang, YY1; Han, C1
刊名: JOURNAL OF BIOLOGICAL CHEMISTRY
发表日期: 2003-06-06
DOI: 10.1074/jbc.M211028200
卷: 278, 期:23, 页:21070-21075
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]: CARDIAC MYOCYTE HYPERTROPHY ; BETA-ADRENERGIC STIMULATION ; ANGIOTENSIN-II ; TRANSCRIPTIONAL ACTIVATION ; PROINFLAMMATORY CYTOKINES ; RECEPTOR STIMULATION ; NITRIC-OXIDE ; RAT-HEART ; EXPRESSION ; FAILURE
英文摘要:

This study was aimed to determine whether beta-adrenergic receptor ( beta-AR) stimulated by isoproterenol (ISO) activates signal transducers and activators of transcription ( STAT) in mouse heart and, if so, to examine the underlying mechanism. We found that treatment of adult male mice by ISO ( 15 mg/kg body weight, intraperitoneal) caused a delayed STAT3 activation ( at 60 120 min), which was fully abolished by beta-AR antagonist, propranolol. ISO-induced phosphorylation of STAT3 was markedly enhanced by phosphodiesterase inhibitor amrinone, indicating that cAMP is critically involved in beta-AR-mediated STAT3 activation. In addition, beta-AR stimulation significantly increased gene expression of interleukin-6 (IL-6) family of cytokines (IL-6, leukemia inhibitory factor, ciliary neurotrophic factor, and cardiotrophin-1). IL-6 protein levels in serum and mouse myocardium were also significantly increased in response to ISO treatment. In cultured cardiac fibroblasts, IL-6 level was enhanced significantly after ISO (10(-6) mol/liter) stimulation for 2 h and then peaked at 12 h, whereas the response of IL-6 in cultured cardiomyocytes to ISO stimulation was not significant, suggesting that ISO-induced increase in IL-6 is primarily from cardiac fibroblasts rather than cardiomyocytes. Most importantly, IL-6 could activate STAT3 in a time-dependent manner in cultured cardiomyocytes, and inhibition of IL-6 level by anti-IL-6-neutralizing antibody clearly attenuated ISO-induced phosphorylation of STAT3 in myocardium. Taken together, these results indicate that beta-AR stimulation leads to a delayed STAT3 activation via an IL-6 family of cytokine-mediated pathway and that cardiac fibroblasts, but not cardiomyocytes, is probably the predominant source of IL-6 in response to ISO stimulation in mouse myocardium.

语种: 英语
WOS记录号: WOS:000183230500081
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51783
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, Inst Vasc Med, Hosp 3, Hlth Sci Ctr, Beijing 100083, Peoples R China
2.Peking Univ, Reference Lab Educ, Minist Mol Cardiol, Hlth Sci Ctr, Beijing 100083, Peoples R China
3.Peking Univ, Inst Cardiovasc Sci, Hlth Sci Ctr, Beijing 100083, Peoples R China

Recommended Citation:
Yin, F,Li, P,Zheng, M,et al. Interleukin-6 family of cytokines mediates isoproterenol-induced delayed STAT3 activation in mouse heart[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2003,278(23):21070-21075.
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