title: Early and transient gene expression changes in pressure overload-induced cardiac hypertrophy in mice.
abstract: Cardiac hypertrophy is an important risk factor for cardiac morbidity and mortality. To unravel the underlying pathogenic genetic pathways, we hybridized left ventricular RNA from Transverse Aortic Constriction mice at 48 h, 1 week, and 2, 3, and 8 weeks after surgery to microarrays containing a 15K fetal cDNA collection. Key processes involved an early restriction in the expression of metabolic genes, accompanied by increased expression of genes related to growth and reactivation of fetal genes. Most of these genes returned to basal expression levels during the later, compensated hypertrophic phase. Our findings suggest that compensated hypertrophy in these mice is established by rapid adaptation of the heart at the cost of gene expression associated with metabolic activity, with only temporary expression of possible maladaptive processes. Therefore, the transient early changes may reflect a beneficial response to pressure overload, as deterioration of cardiac hemodynamic function or heart failure does not occur.
authors.affiliation: Department of Genetics and Cell Biology, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.
authors.forename: B J C
authors.initials: BJ
authors.lastname: van den Bosch
authors.forename: P J
authors.initials: PJ
authors.lastname: Lindsey
authors.forename: C M M
authors.initials: CM
authors.lastname: van den Burg
authors.forename: S A
authors.initials: SA
authors.lastname: van der Vlies
authors.forename: D J
authors.initials: DJ
authors.lastname: Lips
authors.forename: G J
authors.initials: GJ
authors.lastname: van der Vusse
authors.forename: T A
authors.initials: TA
authors.lastname: Ayoubi
authors.forename: P A
authors.initials: PA
authors.lastname: Doevendans
authors.forename: H J M
authors.initials: HJ
authors.lastname: Smeets
mesh_terms: D000818:Animals; D001011:Aorta / Q000601:surgery; D006332:Cardiomegaly / Q000209:etiology / Q000235:genetics*; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000235:genetics; D005786:Gene Expression Regulation; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000235:genetics; D008297:Male; D051379:Mice; D020411:Oligonucleotide Array Sequence Analysis; D017725:Ventricular Pressure