title: Systemic heme oxygenase-1 transgenic overexpression aggravates pressure overload-induced cardiac hypertrophy in mice.
abstract: OBJECTIVE
  Heme oxygenase-1(HO-1) has been reported to protect against cardiac hypertrophy in cultured neonatal cardiomyocytes treated with HO-1 inducer, cardiac specific HO-1 transgenic mice, or animals treated with HO-1 inducer. The aim of the present study is to examine the effects of systemic HO-1 transgenic overexpression on pressure overload-induced cardiac hypertrophy in mice.
  
  
  METHODS
  Pressure-overload cardiac hypertrophy was induced by transverse aortic constriction (TAC) in WT (wild type) and systemic HO-1 transgenic overexpression (TG) mice.
  
  
  RESULTS
  We found that systemic HO-1 transgenic overexpression aggravated pressure overload-induced cardiac hypertrophy. Pressure-overload induced the more increases of heart weight/ body weigh index, left ventricular weight/ body weight index, β-MHC protein expression, cardiac interstitial fibrosis in TG mice than in WT mice. Pressure-overload increased cardiac HO-1 protein expression in WT but not TG mice, but the cardiac HO-1 protein level was still higher in TAC-treated TG mice than in TAC-treated WT mice. The basal cardiac calcineurin protein level in TG mice was lower than that in WT mice. Pressure-overload increased calcineurin protein expression in both WT and TG mice; however, pressure-overload induced more calcineurin protein expression in TG mice than in WT mice.
  
  
  CONCLUSIONS
  This study shows for the first time that systemic HO-1 transgenic overexpression aggravates pressure overload-induced cardiac hypertrophy.
authors.affiliation: Department of Pharmacology, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin Medical University, Harbin, PR China.
authors.forename: Chang
authors.initials: C
authors.lastname: Chen
authors.forename: Rong
authors.initials: R
authors.lastname: Huo
authors.forename: Yan
authors.initials: Y
authors.lastname: Tong
authors.forename: Yue
authors.initials: Y
authors.lastname: Sheng
authors.forename: Hui-Bin
authors.initials: HB
authors.lastname: Liu
authors.forename: Xu
authors.initials: X
authors.lastname: Gao
authors.forename: Osamu
authors.initials: O
authors.lastname: Nakajima
authors.forename: Bao-Feng
authors.initials: BF
authors.lastname: Yang
authors.forename: De-Li
authors.initials: DL
authors.lastname: Dong
mesh_terms: D000818:Animals; D001011:Aorta / Q000503:physiopathology; D019703:Calcineurin / Q000378:metabolism; D006332:Cardiomegaly / Q000201:enzymology* / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D003251:Constriction, Pathologic / Q000503:physiopathology; D004195:Disease Models, Animal; D005355:Fibrosis / Q000209:etiology; D015870:Gene Expression; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism*; D006439:Hemodynamics / Q000502:physiology; D007501:Iron / Q000032:analysis; D051379:Mice; D008822:Mice, Transgenic; D018995:Myosin Heavy Chains / Q000378:metabolism
chemical_list: C551613:Myh7 protein, mouse; D007501:Iron; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; C105245:heme oxygenase-2; D019703:Calcineurin; D018995:Myosin Heavy Chains