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

Nicola J. Smith; Ross D. Hannan; Walter G. Thomas; Rebecca A. Lew

doi:10.1007/BF02442574

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

Nicola J. Smith, Ross D. Hannan, Walter G. Thomas^*, Rebecca A. Lew

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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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.

Original language	English
Pages (from-to)	431-435
Number of pages	5
Journal	Letters in Peptide Science
Volume	10
Issue number	5-6
DOIs	https://doi.org/10.1007/BF02442574
Publication status	Published - Nov 2003
Externally published	Yes

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title = "AngiotensinII mediates cardiomyocyte hypertrophic growth pathways via MMP-dependent HB-EGF liberation",

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.",

keywords = "AngII Type I receptor, Angiotensin II, Cardiac hypertrophy, EGFR, HB-EGF, MMP",

author = "Smith, \{Nicola J.\} and Hannan, \{Ross D.\} and Thomas, \{Walter G.\} and Lew, \{Rebecca A.\}",

year = "2003",

month = nov,

doi = "10.1007/BF02442574",

language = "English",

volume = "10",

pages = "431--435",

journal = "Letters in Peptide Science",

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publisher = "Springer Science+Business Media B.V.",

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}

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T1 - AngiotensinII mediates cardiomyocyte hypertrophic growth pathways via MMP-dependent HB-EGF liberation

AU - Smith, Nicola J.

AU - Hannan, Ross D.

AU - Thomas, Walter G.

AU - Lew, Rebecca A.

PY - 2003/11

Y1 - 2003/11

N2 - 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.

AB - 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.

KW - AngII Type I receptor

KW - Angiotensin II

KW - Cardiac hypertrophy

KW - EGFR

KW - HB-EGF

KW - MMP

UR - https://www.scopus.com/pages/publications/15044346931

U2 - 10.1007/BF02442574

DO - 10.1007/BF02442574

M3 - Article

SN - 0929-5666

VL - 10

SP - 431

EP - 435

JO - Letters in Peptide Science

JF - Letters in Peptide Science

IS - 5-6

ER -

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

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