title: Female rats with severe left ventricle volume overload exhibit more cardiac hypertrophy but fewer myocardial transcriptional changes than males.
abstract: Aortic valve regurgitation (AR) imposes a volume overload (VO) to the left ventricle (LV). Male rats with a pathological heart overload usually progress more quickly towards heart failure than females. We examined whether a sexual dimorphism exists in the myocardial transcriptional adaptations to AR. Adult Wistar male and female rats either underwent a sham operation or were induced with AR and then followed for 26 weeks. Female AR rats gained relatively more LV mass than males (75 vs. 42%). They had a similar increase in LV chamber dimensions compared to males but more wall thickening. On the other hand, fatty acid oxidation (FAO)-related LV enzyme activity was only decreased in AR males. The expression of genes encoding FAO-related enzymes was only reduced in AR males and not in females. A similar situation was observed for the expression of genes involved in mitochondrial biogenesis or function as well as for genes encoding for transcription factors implicated in the control of bioenergetics and mitochondrial function (Errα, Errγ or Pgc1α). Although females develop more LV hypertrophy from severe VO, their myocardial gene expression remains closer to normal. This could provide survival benefits for females with severe VO.
authors.affiliation: Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Quebec City, Canada.
authors.forename: Catherine
authors.initials: C
authors.lastname: Beaumont
authors.affiliation: Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Quebec City, Canada.
authors.forename: Élisabeth
authors.initials: É
authors.lastname: Walsh-Wilkinson
authors.affiliation: Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Quebec City, Canada.
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Drolet
authors.affiliation: Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Quebec City, Canada.
authors.forename: Élise
authors.initials: É
authors.lastname: Roussel
authors.affiliation: Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Quebec City, Canada. marie.arsenault@criucpq.ulaval.ca.
authors.forename: Marie
authors.initials: M
authors.lastname: Arsenault
authors.affiliation: Groupe de recherche sur les valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Quebec City, Canada. jacques.couet@med.ulaval.ca.
authors.forename: Jacques
authors.initials: J
authors.lastname: Couet
mesh_terms: D000818:Animals; D015415:Biomarkers; D001706:Biopsy; D006332:Cardiomegaly / Q000000981:diagnostic imaging / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004452:Echocardiography; D004734:Energy Metabolism; D005260:Female; D006334:Heart Function Tests; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D051381:Rats; D012737:Sex Factors; D014158:Transcription, Genetic; D018487:Ventricular Dysfunction, Left / Q000235:genetics* / Q000503:physiopathology*; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers