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

Figure 4

ROS contributes to the roles of JMJD1A in cardiomyocytes. (a) Jmjd1a knockdown promotes ISO-induced total cellular and mitochondrial ROS. NRCMs were infected with indicated adenovirus for 24 hours and then treated with ISO (1 μM) for 12 hours. vs. PBS+si-NC and ^## vs. ISO+si-NC. (b) JMJD1A overexpression reduces ISO-induced total cellular and mitochondrial ROS. NRCMs were infected with indicated adenovirus for 24 hours and then treated with ISO (1 μM) for 12 hours. vs. PBS+si-NC and ^## vs. ISO+si-NC. (c) NAC and MitoTEMPO repress Jmjd1a knockdown-mediated increase in total and mitochondrial ROS, respectively. NRCMs were transfected with indicated siRNA for 24 hours and then treated with ISO (1 μM) in the presence of NAC (2 mM) or MitoTEMPO (50 nM) for 12 hours. vs. PBS+si-NC and ^## vs. ISO+si-NC. (d) NAC and MitoTEMPO repress Jmjd1a knockdown-mediated increase in cardiomyocyte size. NRCMs were transfected with indicated siRNA for 24 hours and then treated with ISO (1 μM) in the presence of NAC (2 mM) or MitoTEMPO (50 nM) for 48 hours. vs. PBS+si-NC. (e) NAC represses JMJD1A knockdown-mediated increase in expression of hypertrophic fetal genes. NRCMs were transfected with indicated siRNA for 24 hours and then treated with ISO (1 μM) in the presence of NAC (2 mM) for 48 hours. vs. PBS+si-NC. (f) MitoTEMPO represses the JMJD1A knockdown-mediated increase in the expression of hypertrophic fetal genes. NRCMs were transfected with indicated siRNA for 24 hours and then treated with ISO (1 μM) in the presence of MitoTEMPO (50 nM) for 48 hours. vs. PBS+si-NC.

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