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Cross-talk between angiotensin II and interleukin-6-induced signaling through Stat3 transcription factor

G J Bhat1, K M Baker

  • 1Pen State University College of Medicine, Weis Center for Research, Danville, PA 17822, USA.

Basic Research in Cardiology
|January 8, 1999
PubMed

Insights

Angiotensin II (Ang II) delays Stat3 phosphorylation by inducing an inhibitory pathway, unlike IL-6. This Ang II-mediated inhibition of Stat3 activation is reversible and relevant to cardiac hypertrophy and inflammation.

Area of Science:

  • Cellular signaling pathways
  • Molecular biology
  • Cardiovascular research

Background:

  • Angiotensin II (Ang II) is a key regulator of cardiovascular function.
  • Signal Transducers and Activators of Transcription (Stat) proteins are crucial in cellular responses.
  • Interleukin-6 (IL-6) is a cytokine involved in inflammation and acute phase responses.

Purpose of the Study:

  • To investigate the mechanism behind Ang II-induced delayed Stat3 tyrosine phosphorylation.
  • To test the hypothesis that Ang II induces an inhibitory pathway before Stat3 activation.
  • To explore the cross-talk between Ang II and IL-6 signaling pathways.

Main Methods:

  • Utilized cultured neonatal rat cardiac fibroblasts and CHO-K1 cells expressing Ang II type 1 receptors (T3CHO/AT1A).
  • Compared Stat3 tyrosine phosphorylation kinetics induced by Ang II versus IL-6.
  • Assessed the effect of Ang II on IL-6-induced Stat3 phosphorylation.
  • Investigated the role of MAP kinase kinase 1 (MAPKK1) using the inhibitor PD98059.

Main Results:

  • Ang II induced a delayed Stat3 tyrosine phosphorylation, peaking at 2 hours, contrasting with IL-6's rapid effect (15-30 min).
  • Short Ang II treatment transiently inhibited IL-6-induced Stat3 tyrosine phosphorylation.
  • The inhibitory effect of Ang II on Stat3 phosphorylation was attenuated by PD98059, suggesting MAPKK1 involvement.

Conclusions:

  • Ang II delays Stat3 activation by inducing a transient inhibitory pathway, likely involving MAPKK1.
  • Modulatory cross-talk between Ang II and IL-6 signaling pathways exists.
  • These interactions may be significant in conditions like cardiac hypertrophy and inflammatory responses.

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