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Transgenic mice with cardiac-specific expression of activating transcription factor 3, a stress-inducible gene, have conduction abnormalities and contractile dysfunction.

Authors: Okamoto, Y  Chaves, A  Chen, J  Kelley, R  Jones, K  Weed, HG  Gardner, KL  Gangi, L  Yamaguchi, M  Klomkleaw, W  Nakayama, T  Hamlin, RL  Carnes, C  Altschuld, R  Bauer, J  Hai, T 
Citation: Okamoto Y, etal., Am J Pathol. 2001 Aug;159(2):639-50.
Pubmed: (View Article at PubMed) PMID:11485922
DOI: Full-text: DOI:10.1016/S0002-9440(10)61735-X

Activating transcription factor 3 (ATF3) is a member of the CREB/ATF family of transcription factors. Previously, we demonstrated that the expression of the ATF3 gene is induced by many stress signals. In this report, we demonstrate that expression of ATF3 is induced by cardiac ischemia coupled with reperfusion (ischemia-reperfusion) in both cultured cells and an animal model. Transgenic mice expressing ATF3 under the control of the alpha-myosin heavy chain promoter have atrial enlargement, and atrial and ventricular hypertrophy. Microscopic examination showed myocyte degeneration and fibrosis. Functionally, the transgenic heart has reduced contractility and aberrant conduction. Interestingly, expression of sorcin, a gene whose product inhibits the release of calcium from sarcoplasmic reticulum, is increased in these transgenic hearts. Taken together, our results indicate that expression of ATF3, a stress-inducible gene, in the heart leads to altered gene expression and impaired cardiac function.

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CRRD Object Information
CRRD ID: 7327201
Created: 2013-09-16
Species: All species
Last Modified: 2013-09-16
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.