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AngiotensinII mediates cardiomyocyte hypertrophic growth pathways via MMP-dependent HB-EGF liberation

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Abstract

Pathological cardiac stimulation by angiotensinII (AngII) can cause left ventricular hypertrophy, a major independent risk factor for heart attack and death. We have previously reported that AngII exerts its hypertrophic effects by usurping the epidermal growth factor (EGF) signalling pathway via metalloprotease-dependent transactivation. However, the EGF-like ligand responsible for AngII-mediated transactivation and cardiac hypertrophy remains to be identified. Using phosphorylated ERK1/2 as a read-out of growth pathway activation and an alkaline phosphatase-tagged Heparin-Binding EGF-like Growth Factor (HB-EGF) reporter construct to examine AngII-mediated liberation, we provide evidence that HB-EGF is the soluble growth factor involved in AngII-induced left ventricular hypertrophy.

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Authors and Affiliations

  1. Baker Heart Research Institute, Melbourne, Victoria, Australia

    Nicola J. Smith, Walter G. Thomas & Rebecca A. Lew

  2. Department of Pharmacology, University of Melbourne, Melbourne, Victoria, Australia

    Nicola J. Smith

  3. Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

    Ross D. Hannan

Authors
  1. Nicola J. Smith
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  2. Ross D. Hannan
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  3. Walter G. Thomas
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  4. Rebecca A. Lew
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Smith, N.J., Hannan, R.D., Thomas, W.G. et al. AngiotensinII mediates cardiomyocyte hypertrophic growth pathways via MMP-dependent HB-EGF liberation. Int J Pept Res Ther 10, 431–435 (2003). https://doi.org/10.1007/s10989-004-2398-3

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  • DOI: https://doi.org/10.1007/s10989-004-2398-3

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