KLF15 and PPARα Cooperate to Regulate Cardiomyocyte Lipid Gene Expression and Oxidation
Ligand induced PPARα lipid oxidation is KLF15 dependent. Oxygen consumption rate (pmol/min) in neonatal rat ventricular cardiomyocytes after sh-RNA mediated Klf15 silencing in the absence or presence of the PPARα-specific ligand WY-14,643 (10 μM, 24 hrs). Arrows along -axis indicate acute addition of BSA-conjugated palmitate (Pal, 150 nM), ATP synthase inhibitor oligomycin (Oligo, 2.5 μg/mL), uncoupler FCCP (1.5 μM), complex III inhibitor antimycin A (4 μM)/complex I inhibitor rotenone (2 μM) (Anti-A/Roten). Inset: maximal oxygen consumption rate at t = 40 min following addition of uncoupler FCCP (n = 6–9). versus vehicle. versus sh-KLF15. versus WY-14643. Values normalized to total cellular protein.