JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase

Figure 5

JMJD1A regulates catalase to modulate ROS and cardiomyocyte hypertrophy. (a) mRNA levels of oxidative genes and antioxidants in cardiomyocytes transfected with/without si-Jmjd1a. NRCMs were transfected with indicated siRNA for 36 hours. vs. si-NC. (b) Protein levels of Catalase in cardiomyocytes transfected with/without si-Jmjd1a. NRCMs were transfected with indicated siRNA for 36 hours. (c) JMJD1A overexpression promotes the expression of Catalase under basal and ISO-induced stress. NRCMs were infected with indicated adenovirus for 24 hours and then treated with ISO (1 μM) for an additional 24 hours. vs. Ad-Ctrl. (d) JMJD1A controls Catalase activity. Cardiomyocytes were treated as in (a) or (c), then, catalase activity in cardiomyocytes was analyzed with a kit. (e) Representative western blot results showing Catalase knockdown in cardiomyocytes. NRCMs were transfected with indicated siRNA for 36 hours. (f) Catalase knockdown blocked JMJD1A-mediated repression in cardiomyocyte hypertrophy. NRCMs were infected with indicated adenovirus for 24 hours and then transfected with si-NC or si-Catalase for 24 hours, followed by ISO (1 μM) treatment for an additional 48 hours. vs. ISO+si-NC+Ad-Ctrl and ^## vs. ISO+si-NC+Ad-Jmjd1a. (g) Catalase knockdown blocked JMJD1A-mediated repression of protein synthesis. The cells were treated as in (e). vs. ISO+si-NC+Ad-Ctrl and ^## vs. ISO+si-NC+Ad-Jmjd1a. (h) Catalase knockdown blocks JMJD1A-mediated repression of the expression of hypertrophic fetal genes. The cells were treated as in vs. ISO+si-NC+Ad-Ctrl and ^## vs. ISO+si-NC+Ad-Jmjd1a.

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