MOESM1 of MiR-30c/PGC-1β protects against diabetic cardiomyopathy via PPARα

Additional file 1: Figure S1. Different expression genes belonging to PPAR family between diabetic hearts and normal ones. Figure S2. High palmitate treatment impaired the insulin signal of NRCMs. Figure S3. The efficacy of siRNAs against PGC-1β. Figure S4. Identification of the primary neonatal rat cardiomyocytes. Figure S5. PGC-1β knockdown relieved high palmitate induced lipotoxicity in vitro. Figure S6. The effects of PGC-1β knockdown on mitochondrial biogenesis and membrane potentials. Figure S7. Overexpression of miR-30c alleviated high palmitate induced lipotoxicity in vitro. Figure S8. The effect of miR-30c on mitochondrial biogenesis and membrane potentials. Figure S9. The effects of rAAV9 mediated miR-30c/anti-miR-30c delivery on plasma lipid profile and blood glucose in vivo. Figure S10. The effects of rAAV9 mediated miR-30c/anti-miR-30c delivery on liver steatosis in vivo. Table S1. The wildtype sequence containing predicted miR-30c binding site of the human PGC-1β 3′ UTR and corresponding mutant sequence. Table S2. Sequences of miR-30c, anti-miR-30c, or miR-random inserted into rAAV expression plasmid. Table S3. Primers of CD36 and PDK4 promotors in ChIP-PCR. Table S4. Primers of rat 12S ribosomal DNA, COI and and 18S ribosomal DNA in real-time PCR. Table S5. Comparison of hemodynamic variables among mice with different treatments.