Journal
JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
Volume 16, Issue 1, Pages 79-91Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1470320313483845
Keywords
Angiotensin II; angiotensin II type 2 receptor; ATIP; cardiac hypertrophy; ERK phosphorylation
Categories
Funding
- Austin Medical Research Foundation
- University of Melbourne
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Hypothesis: Cardiac hypertrophy in myocytes is in part regulated by changes in expression of a novel Ang II type 2 receptor (AT2-receptor) interacting protein identified as ATIP. Introduction: The role of the AT2-receptor in cardiac hypertrophy is controversial, with some reports indicating that AT2-receptor activation has detrimental effects on disease progression, whereas others indicate that it has a beneficial role. Materials and methods: In an effort to unravel this paradox, we examined the expression and function of ATIP in cell-based models of cardiac hypertrophy using QPCR, immunohistochemistry, cell proliferation, morphological and transfection techniques in H9c2 cardio-myoblast and myotubules. Results: These studies indicate that in cultured cardio-myoblast and myotubules, Ang II mediates cellular hypertrophy and proliferation solely via the AT1-receptor, the ATIP variants are abundantly expressed and that ATIP3 may play an anti-proliferative/hypertrophic role in these cells in the absence of AT2-receptor expression or activation. Conclusions: Previously ATIP has been shown to inhibit growth factor signalling in cancerous cells via an interaction with the AT2-receptor. This is the first report to identify that ATIP may have a similar role in other disease states characterised by excessive growth and indicates that for ATIP3, at least, an interaction with the AT2-receptor may not be necessary.
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