Regular Article
Angiotensin II Activates the Proinflammatory Transcription Factor Nuclear Factor-κB in Human Monocytes

https://doi.org/10.1006/bbrc.1999.0543Get rights and content

Abstract

The renin-angiotensin system may contribute to the pathogenesis of atherosclerosis. A common feature of all stages of atherosclerosis is inflammation of the vessel wall. The transcription factor nuclear factor-κB (NF-κB) participates in most signaling pathways involved in inflammation. This study therefore examined the effect of angiotensin (ANG) II on NF-κB activation in monocytic cells, a major cellular component of human atheroma, by electrophoretic mobility shift assay. ANG II, like TNFα, caused rapid activation of NF-κB in human mononuclear cells isolated from peripheral blood by Ficoll density gradient. This ANG II effect was blocked by the angiotensin AT1 receptor antagonist losartan. Specificity of ANG II-induced NF-κB activation was ascertained by supershift and competition experiments. Moreover, ANG II stimulated NF-κB activation in human monocytes, but not in lymphocytes from the same preparation. Together, the data demonstrate the ability of the vasoactive peptide ANG II to activate inflammatory pathways in human monocytes.

References (21)

  • M. Bond et al.

    FEBS Lett.

    (1998)
  • J. Yao et al.

    J. Biol. Chem.

    (1997)
  • A.W. Hahn et al.

    FEBS Lett.

    (1994)
  • E.M. Lonn et al.

    Circulation

    (1994)
  • R. Ross

    N. Engl. J. Med.

    (1999)
  • T. Collins

    Lab. Invest.

    (1993)
  • R. Ross et al.

    Science

    (1990)
  • E. Brogi et al.

    J. Clin. Invest.

    (1993)
  • S.E. Hughes et al.

    Cardiovasc. Res.

    (1993)
  • S.K. Clinton et al.

    Arch. Pathol. Lab. Med.

    (1992)
There are more references available in the full text version of this article.

Cited by (0)

1

Address for correspondence: Department of Cardiology, University of Heidelberg, Bergheimer Str. 58, 69115 Heidelberg, Germany. Fax: +49-6221-565515. E-mail:[email protected].

View full text