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

Motoaki Sano, Keiichi Fukuda, Hiroaki Kodama, Toshiyuki Takahashi, Takahiro Kato, Daihiko Hakuno, Toshihiko Sato, Tomohiro Manabe, Satoko Tahara, Satoshi Ogawa

Research output: Contribution to journalArticlepeer-review

51 Citations (Scopus)


We recently reported that angiotensin II (AngII) biphasically activates the JAK/STAT pathway and induces delayed phosphorylation of STAT3 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.

Original languageEnglish
Pages (from-to)798-802
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - 2000 Mar 24


  • Angiotensin II
  • Autocrine/paracrine
  • STAT3
  • Signal transduction
  • gp130

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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