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. 2017 Jun 30;7:4476. doi: 10.1038/s41598-017-04762-x

Figure 6.

Figure 6

Rarres2 is regulated by MEF2. (a) Expression of Mef2a and Rarres2 in RNA-seq analysis of MEF2A depleted cardiomyocytes (fragments per kilobase of exon per million fragments mapped). (b) ChIP-qPCR analysis demonstrates that MEF2A is recruited to the Rarres2 promoter in primary cardiomyocytes. Data are presented as fold enrichment (n = 3, **P < 0.01). Acta2 was used as a negative control. (c) Rarres2 expression is negatively regulated by MEF2 in a p38 MAPK dependent manner. Primary cardiomyocytes were transfected with siRNA targeting MEF2A, MEF2D or a scrambled siRNA control and treated with SB 203580 (5 μM) for 24 hours. Control cells were treated with an inactive analogue, SB 202474. Data were normalized to Gapdh and are presented as fold change using the delta delta Ct method (n = 3, **P < 0.01, ***P < 0.001). (d) Phosphorylation defective mutated MEF2A prevents Rarres2 induction by p38 inhibition. Primary cardiomyocytes were transfected with empty vector (pcDNA3) or a mutated MEF2A expression construct (T312, 319A) and treated with SB 203580 or SB 202474 (5 μM) for 24 hours. Data were analyzed as in 6c (n = 3, **P < 0.01). (e) Isoproterenol (Iso; 10 μM) treatment for 24 hours, upregulates Rarres2 expression. Data were normalized to Gapdh and are presented as fold change as in 6c (n = 3, **P < 0.01).