| First Author | Saadane N | Year | 2000 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 278 |
| Issue | 3 | Pages | H796-805 |
| PubMed ID | 10710348 | Mgi Jnum | J:61294 |
| Mgi Id | MGI:1354654 | Doi | 10.1152/ajpheart.2000.278.3.H796 |
| Citation | Saadane N, et al. (2000) Altered molecular response to adrenoreceptor-induced cardiac hypertrophy in Egr-1-deficient mice. Am J Physiol Heart Circ Physiol 278(3):H796-805 |
| abstractText | 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. |
