title: Left and right ventricle late remodeling following myocardial infarction in rats.
abstract: The mechanisms involved in cardiac remodeling in left (LV) and right ventricles (RV) after myocardial infarction (MI) are still unclear. We assayed factors involved in collagen turnover in both ventricles following MI in rats either presenting signs of heart failure (pulmonary congestion and increased LVEDP) or not (INF-HF or INF, respectively).
  
  
  
  MI was induced in male rats by ligation of the left coronary artery. Four weeks after MI gene expression of collagen I, connective tissue growth factor (CTGF), transforming growth factor β (TGF-β) and lysyl oxidase (LOX), metalloproteinase-2 (MMP2) and tissue inhibitor metalloproteinase-2 (TIMP2) as well as cardiac hemodynamic in both ventricles were evaluated.
  
  
  
  Ventricular dilatation, hypertrophy and an increase in interstitial fibrosis and myocyte size were observed in the RV and LV from INF-HF animals, whereas only LV dilatation and fibrosis in RV was present in INF. The LV fibrosis in INF-HF was associated with higher mRNA of collagen I, CTGF, TGF-β and LOX expressions than in INF and SHAM animals, while MMP2/TIMP2 mRNA ratio did not change. RV fibrosis in INF and INF-HF groups was associated with an increase in LOX mRNA and a reduction in MMP2/TIMP2 ratio. CTGF mRNA was increased only in the INF-HF group.
  
  
  
  INF and INF-HF animals presented different patterns of remodeling in both ventricles. In the INF-HF group, fibrosis seems to be consequence of collagen production in LV, and by reductions in collagen degradation in RV of both INF and INF-HF animals.
authors.affiliation: Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
authors.forename: Ivanita
authors.initials: I
authors.lastname: Stefanon
authors.forename: María
authors.initials: M
authors.lastname: Valero-Muñoz
authors.forename: Aurélia Araújo
authors.initials: AA
authors.lastname: Fernandes
authors.forename: Eduardo Hertel
authors.initials: EH
authors.lastname: Ribeiro
authors.forename: Cristina
authors.initials: C
authors.lastname: Rodríguez
authors.forename: Maria
authors.initials: M
authors.lastname: Miana
authors.forename: José
authors.initials: J
authors.lastname: Martínez-González
authors.forename: Jessica S
authors.initials: JS
authors.lastname: Spalenza
authors.forename: Vicente
authors.initials: V
authors.lastname: Lahera
authors.forename: Paula F
authors.initials: PF
authors.lastname: Vassallo
authors.forename: Victoria
authors.initials: V
authors.lastname: Cachofeiro
mesh_terms: D000818:Animals; D003094:Collagen / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005355:Fibrosis; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006439:Hemodynamics; D007249:Inflammation / Q000235:genetics / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D020257:Ventricular Remodeling / Q000235:genetics
chemical_list: D003094:Collagen