[Effects of ZFP580 on ventricular remodeling after myocardial ischemia/reperfusion in rats]

To investigate the relationship between zinc finger protein(ZFP580)and ventricular remodeling after myocardial is-chemia/reperfusion(I/R) injury in rats.

Seventy-two rats were divided into sham group and I/R groups which would be tested in se-ries time of 0.5 h, 1 h, 2 h, 4 h, 1 d,7 d,14 d,28 d after reperfusion to observe the expression of ZFP580 in rat myocardium. The H9C2 cells were cultured and treated with transforming growth factor-beta1 (TGF-β 1) to establish cardiac hypertrophy in vitro model in series time of 0 h, 8h, 16 h and 24 h. The cardiomyocyte hypertrophy morphology was measured. The mRNA levels of atrial natriuretic peptide(ANP), myosin heavey chain beta(β -MHC) and ZFP580 genes were quantified. The protein levels of MMP-3 and ZFP580 were quantified after H9C2 cells were transfected by lentiviral-mediated ZFP580 gene.

Myocardial I/R injury model was successfully established. Myocardial tis-sue in rats had large area infarction, and myocardial cells were eosinophilic changed. The increased level of ZFP580 protein was observed in the cardiomyocytes around infarction zone. The expression of TGF-β 1 in myocardium was up-regulated after myocardial I/R injury. TGF-β 1 (5 ng/ml) treatment could induce cardiomyocyte hypertrophy in H9C2 cells. TGF-β 1 treatment increased the cell size and mRNA levels of ANP andβ -MHC genes (P < 0.05), which represent degree of cardiac hypertrophy. TGF-β 1 treatment also increased the protein levels of ZFP580 in H9C2 cells (P < 0.05). In the H9C2 cells transfected by lentiviral-mediated gene, the protein level of MMP3 was decreased (P < 0.05).

ZFP580 is probably related with ventricular remodeling after myocardial I/R injury by involving TGF-β 1 induced cardiomyocyte hypertrophy and attenuating MMP-3 production.