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.

journal_name

Genomics

journal_title

Genomics

authors

van den Bosch BJ,Lindsey PJ,van den Burg CM,van der Vlies SA,Lips DJ,van der Vusse GJ,Ayoubi TA,Doevendans PA,Smeets HJ

doi

10.1016/j.ygeno.2006.04.012

subject

Has Abstract

pub_date

2006-10-01 00:00:00

pages

480-8

issue

4

eissn

0888-7543

issn

1089-8646

pii

S0888-7543(06)00138-8

journal_volume

88

pub_type

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