TAFII250, Egr-l, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin

Citation
N. Saadane et al., TAFII250, Egr-l, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin, AM J P-HEAR, 45(3), 1999, pp. H803-H814
Citations number
59
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
45
Issue
3
Year of publication
1999
Pages
H803 - H814
Database
ISI
SICI code
0363-6135(199903)45:3<H803:TEADCE>2.0.ZU;2-U
Abstract
Differential display identified that gene fragment HA220 homologous to the transcriptional activator factor II 250 (TAFII250) gene, or CCG1, was incre ased in hypertrophied rodent heart. To determine whether TAFII250 gene expr ession is modified after cardiac damage, we measured TAFII250 expression in vivo in mouse hearts after injection of the cardiotoxic agent doxorubicin (DXR) and in vitro in DXR-treated isolated rat neonatal cardiomyocytes. In vivo atrial naturetic factor (ANF), beta-myosin heavy chain (beta-MHC), Egr -1, and TAFII250 expression increased with dose and time after a single DXR injection, but only ANF and beta-MHC expression were increased after multi ple injections. After DXR treatment of neonatal cardiomyocytes we found dec reased ANF, alpha-MHC, Egr-1, and TAFII250 expression. Expression of the TA FII250-regulated genes, the D-type cyclins, was increased after a single in jection in adult mice and was decreased in DXR-treated cardiomyocytes. Thus expression of Erg-l, TAFII250, and the D-type cyclins is modulated after c ardiotoxic damage in adult and neonatal heart.