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Am J Physiol Heart Circ Physiol 278: H796-H805, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 3, H796-H805, March 2000

Altered molecular response to adrenoreceptor-induced cardiac hypertrophy in Egr-1-deficient mice

Nacéra Saadane1, Lesley Alpert2, and Lorraine E. Chalifour1,3

1 Lady Davis Institute for Medical Research and 2 Department of Pathology, Sir Mortimer B. Davis-Jewish General Hospital, Montreal H3T 1E2; and 3 Division of Experimental Medicine, Department of Medicine, McGill University, Montreal, Quebec, Canada H3A 1A3

Unmanipulated early growth response-1 (Egr-1)-deficient -/- mice have similar heart-to-body weight ratios but express lower amounts of atrial natriuretic factor (ANF), beta -myosin heavy chain (beta -MHC), skeletal actin, NGF1-A binding protein (NAB)-2, Sp1, c-fos, c-jun, GATA-4, and Nkx2.5 than +/+ or +/- mice. alpha -MHC, tubulin, and NAB-1 expression was similar. Isoproterenol (Iso) and phenylephrine (PE) infusion into +/+ and -/- mice increased heart weight, ANF, beta -MHC, skeletal actin, Sp1, NAB-2, c-fos, and c-jun expression, but induction in -/- mice was lower. Only Iso + PE-treated +/+ mice showed induction of NAB-1, GATA-4, and Nkx2.5. Foci of fibrosis were found in Iso + PE-treated -/- and +/+ mice. Surprisingly, vehicle-treated -/- mice displayed fibrosis and increased Sp1, skeletal actin, Nkx2.5, and GATA-4 expression without hypertrophy. Minipump removal caused the agonist-treated hearts and gene expression to regress to control or near-control levels. Thus Egr-1 deficiency caused a blunted catecholamine-induced hypertrophy response and increased sensitivity to stress.

catecholamines; gene expression


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