title: Overexpression of apolipoprotein B attenuates pathologic cardiac remodeling and hypertrophy in response to catecholamines and after myocardial infarction in mice.
abstract: BACKGROUND
  The heart produces apolipoprotein (apo) B-containing lipoproteins which enables cardiac export of potentially cardiotoxic lipids. We hypothesized that overexpression of apoB attenuates the pathologic cardiac remodeling and hypertrophic response following pathological stimuli such as chronic adrenergic overstimulation and myocardial infarction (MI).
  
  
  METHODS
  Cardiac hypertrophy was induced by a chronic infusion of isoproterenol (ISO) 15 mg/kg/day for 3 weeks in human apoB transgenic mice (n = 9) and in non-transgenic wild-type mice (n = 10). As controls, apoB transgenic (n = 10) and wild-type mice (n = 10) saline infusions were used. Transthoracic echocardiography was performed at baseline and after 3 weeks of treatment to evaluate left ventricular (LV) function and morphology. To investigate the effects of expression on postinfarct hypertrophic response we induced MI in apoB transgenic mice (n = 8) and in wild-type controls (n = 11). The hearts were explanted and weighed 6 weeks post MI.
  
  
  RESULTS
  At baseline, WT mice had higher BW and LV mass (LVM) compared to the apoB mice. The increase in LV mass and dimensions after 3 weeks of treatment with ISO was significantly lower while systolic function was significantly better in the apoB group. Six weeks post MI the apoB mice had significantly lower heart weight and heart weight to body weight ratio. The infarct size was similar in both groups.
  
  
  CONCLUSIONS
  Overexpression of apoB attenuates the pathologic remodeling and hypertrophic response to chronic adrenergic stimulation and MI. Our results indicate that cardiac expression of apoB-containing lipoproteins might be an important regulator of myocardial structure and function.
authors.affiliation: Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. truls@wlab.gu.se
authors.forename: Truls
authors.initials: T
authors.lastname: Råmunddal
authors.forename: Malin
authors.initials: M
authors.lastname: Lindbom
authors.forename: Margareta Scharin
authors.initials: MS
authors.lastname: Täng
authors.forename: Yangzhen
authors.initials: Y
authors.lastname: Shao
authors.forename: Jan
authors.initials: J
authors.lastname: Borén
authors.forename: Elmir
authors.initials: E
authors.lastname: Omerovic
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000096:biosynthesis*; D006332:Cardiomegaly / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D007545:Isoproterenol; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D016277:Ventricular Function, Left / Q000187:drug effects; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D001055:Apolipoproteins B; D007545:Isoproterenol