title: Function and expression of ATIP and its variants in cardiomyoblast cell line H9c2.
abstract: OBJECTIVE
  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.
  
  
  BACKGROUND
  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.
  
  
  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.
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
authors.forename: Naghmeh
authors.initials: N
authors.lastname: Varghayee
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Krezel
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
authors.forename: Linda
authors.initials: L
authors.lastname: Rezmann
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
authors.forename: Laurie
authors.initials: L
authors.lastname: Chow
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
authors.forename: Albert George
authors.initials: AG
authors.lastname: Frauman
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia.
authors.forename: William J
authors.initials: WJ
authors.lastname: Louis
authors.affiliation: Clinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Australia simonnsl@unimelb.edu.au.
authors.forename: Simon N
authors.initials: SN
authors.lastname: Louis
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism; D002460:Cell Line; D049109:Cell Proliferation; D048429:Cell Size; D005822:Genetic Vectors; D047908:Intracellular Signaling Peptides and Proteins / Q000096:biosynthesis* / Q000502:physiology*; D018485:Muscle Fibers, Skeletal / Q000378:metabolism; D032386:Myoblasts, Cardiac / Q000378:metabolism*; D010766:Phosphorylation; D051381:Rats; D044139:Receptor, Angiotensin, Type 2 / Q000378:metabolism; D013936:Thymidine / Q000378:metabolism
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; C560086:Mtus1 protein, rat; D044139:Receptor, Angiotensin, Type 2; D013936:Thymidine
keywords: ATIP; Angiotensin II; ERK phosphorylation; angiotensin II type 2 receptor; cardiac hypertrophy