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|Title:||Function and expression of ATIP and its variants in cardiomyoblast cell line H9c2.|
|Authors:||Varghayee, Naghmeh;Krezel, Michael A;Rezmann, Linda Adriana;Chow, Laurie T C;Frauman, Albert G;Louis, William J;Louis, Simon N S|
|Affiliation:||Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia|
Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia email@example.com.
|Citation:||Journal of the Renin-angiotensin-aldosterone System : Jraas 2013; 16(1): 79-91|
|Abstract:||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.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.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.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.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.|
|Internal ID Number:||23559668|
angiotensin II type 2 receptor
|Appears in Collections:||Journal articles|
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