Key result
ZFP580 modulates post-reperfusion remodeling by promoting TGF-β1-induced cardiomyocyte hypertrophy and reducing MMP-3 production.
Why the study?
The relationship between zinc finger protein ZFP580 and ventricular remodeling after myocardial ischemia/reperfusion injury in rats was not well understood.
p-value: p=< 0.05
ZFP580 may play a role in ventricular remodeling after myocardial ischemia/reperfusion injury by modulating TGF-β1 induced hypertrophy and MMP-3 production.
ZFP580 changes post-I/R may link to remodeling; hypothesis-generating and leaves clinical relevance open.
OBJECTIVE: To investigate the relationship between zinc finger protein(ZFP580)and ventricular remodeling after myocardial is-chemia/reperfusion(I/R) injury in rats. METHODS: 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. RESULTS: < 0.05). CONCLUSIONS: 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.
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Meng et al. (2017) studied Myocardial ischemia/reperfusion injury and ventricular remodeling (n=72). Myocardial ischemia/reperfusion and lentiviral-mediated ZFP580 gene transfection vs. Sham group / untreated cells was evaluated on Expression of ZFP580, cardiomyocyte hypertrophy morphology, mRNA levels of ANP, β-MHC, and protein levels of MMP-3 (p=< 0.05). ZFP580 is likely related to ventricular remodeling after myocardial ischemia/reperfusion injury by involving TGF-β1 induced cardiomyocyte hypertrophy and attenuating MMP-3 production (P<0.05).
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