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

Citation
M. Sano et al., Autocrine/paracrine secretion of IL-6 family cytokines causes angiotensin II-induced delayed STAT3 activation, BIOC BIOP R, 269(3), 2000, pp. 798-802
Citations number
22
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN journal
0006-291X → ACNP
Volume
269
Issue
3
Year of publication
2000
Pages
798 - 802
Database
ISI
SICI code
0006-291X(20000324)269:3<798:ASOIFC>2.0.ZU;2-N
Abstract
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 phosphor ylation of STAT3 at 5 min. This delayed phosphorylation was almost complete ly inhibited by anti-gp130 blocking antibody RX435, but not by TAK044 (ET-A /B-R antagonist), prazosin, or propranolol. AngII induced phosphorylation o f gp130 in the late stage, which was temporally in parallel with the delaye d phosphorylation of STAT3. AngII augmented IL-6, CT-1, and LIF mRNA expres sion at 30-60 min, but not CNTF expression, AngII increased IL-6 protein le vels by 3-fold in the conditioned media at 2 h compared with the control. T hese findings indicated that AngII-induced delayed activation of STAT3 is c aused by autocrine/paracrine secreted IL-6 family cytokines. (C) 2000 Acade mic Press.