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

Smith, Nicola J., Hannan, Ross D., Thomas, Walter G. and Lew, Rebecca A. (2003) Angiotensin II mediates cardiomyocyte hypertrophic growth pathways via MMP-dependent HB-EGF liberation. Letters in Peptide Science, 10 5: 431-435.


Author Smith, Nicola J.
Hannan, Ross D.
Thomas, Walter G.
Lew, Rebecca A.
Title Angiotensin II mediates cardiomyocyte hypertrophic growth pathways via MMP-dependent HB-EGF liberation
Journal name Letters in Peptide Science   Check publisher's open access policy
ISSN 0929-5666
Publication date 2003
Year available 2003
Sub-type Article (original research)
DOI 10.1007/s10989-004-2398-3
Volume 10
Issue 5
Start page 431
End page 435
Total pages 5
Place of publication Leiden, The Netherlands
Publisher Kluwer
Language eng
Subject 060110 Receptors and Membrane Biology
060111 Signal Transduction
060199 Biochemistry and Cell Biology not elsewhere classified
060108 Protein Trafficking
060602 Animal Physiology - Cell
110201 Cardiology (incl. Cardiovascular Diseases)
110903 Central Nervous System
Abstract 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.
Keyword Angiotensin II
AngII Type I receptor
EGFR
EGFR
HB-EGF
MMP
Cardiac hypertrophy
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Biomedical Sciences Publications
 
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