The effect of TAZ-K in neonatal rat cardiomyocytes. Rattus norvegicus

Accumulating evidence suggests that new cardiomyocytes are generated from existing cardiomyocytes at a low rate throughout life. This limited regenerative capacity is unable to restore cardiac function after substantial cardiac damage; thus, small molecules have been examined for their ability to enhance the replication of existing cardiomyocytes. A novel compound TAZ-K promoted cardiomyocyte proliferation, therefore, we analyzed the effect of TAZ-K on gene expression in neonatal rat cardiomyocytes. Gene expression involved in cell cycle, anti-oxidant and anti-apoptosis was up-regulated. Thus, TAZ-K may have multifaceted effects and provide a treatment strategy that complements current therapies for patients with myocardial infarction. Overall design: Primary neonatal rat cardiomyocytes were cultured in DMEM media supplemented with 10% FCS. After 24 hours, cardiomyocytes were starved (0.1% FCS) for 6 hours, subsequently treated with vehicle (3 samples) or TAZ-K (10 µM; 3 samples) for 24 hours. Cardiomyocytes were harvested, and total RNA was isolated and utilized for gene expression analysis.