Autocrine/paracrine secretion of IL-6 family cytokines causes angiotensin II-induced delayed STAT3 activation

被引：49

作者：

Sano, M ^{[1
]}

Fukuda, K ^{[1
]}

Kodama, H ^{[1
]}

Takahashi, T ^{[1
]}

Kato, T ^{[1
]}

Hakuno, D ^{[1
]}

Sato, T ^{[1
]}

Manabe, T ^{[1
]}

Tahara, S ^{[1
]}

Ogawa, S ^{[1
]}

机构：

[1] Keio Univ, Dept Internal Med, Cardiopulm Div, Shinjuku Ku, Tokyo 1608582, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2000年 / 269卷 / 03期

基金：

日本学术振兴会;

关键词：

angiotensin II; STAT3; gp130; autocrine/paracrine; signal transduction;

D O I：

10.1006/bbrc.2000.2364

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We recently reported that angiotensin II (AngII) biphasically activates the JAK/STAT pathway and induces delayed phosphorylation of STATS in the late stage (120 min) in cardiomyocytes. This study was designed to determine the mechanism of delayed phosphorylation of STAT3. Conditioned medium prepared from AngII-stimulated cardiomyocytes could reproduce the tyrosine phosphorylation of STAT3 at 5 min. This delayed phosphorylation was almost completely inhibited by anti-gp130 blocking antibody RX435, but not by TAK044 (ET-A/B-R antagonist), prazosin, or propranolol. AngII induced phosphorylation of gp130 in the late stage, which was temporally in parallel with the delayed phosphorylation of STAT3. AngII augmented IL-6, CT-1, and LIF mRNA expression at 30-60 min, but not CNTF expression, AngII increased IL-6 protein levels by 3-fold in the conditioned media at 2 h compared with the control. These findings indicated that AngII-induced delayed activation of STAT3 is caused by autocrine/paracrine secreted IL-6 family cytokines. (C) 2000 Academic Press.

引用

页码：798 / 802

页数：5

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