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
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.