Document Detail

Function and expression of ATIP and its variants in cardiomyoblast cell line H9c2.
MedLine Citation:
PMID:  23559668     Owner:  NLM     Status:  Publisher    
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.
Naghmeh Varghayee; Michael A Krezel; Linda Rezmann; Laurie Chow; Albert George Frauman; William J Louis; Simon N Louis
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-4-4
Journal Detail:
Title:  Journal of the renin-angiotensin-aldosterone system : JRAAS     Volume:  -     ISSN:  1752-8976     ISO Abbreviation:  J Renin Angiotensin Aldosterone Syst     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-4-5     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100971636     Medline TA:  J Renin Angiotensin Aldosterone Syst     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
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