FIGURE 9.

Lack of Plin5 promotes FA oxidation in cardiomyocytes. A, expression of perilipin family proteins and fatty acid oxidation enzymes in the hearts of wild-type mice before and after birth. VLCAD, very long-chain acyl-CoA dehydrogenase, and MCAD, medium-chain acyl-CoA dehydrogenase. B, expression of perilipin family proteins, lipases, and fatty acid-oxidizing enzymes in cardiomyocytes after the culture for 2 days in the presence of oleic acid (see “Experimental Procedures”). Cardiomyocytes prepared from the hearts of eight wild-type and Plin5^−/− mice 3 days after birth were seeded in three culture dishes, respectively. Arrowhead, correct band of Plin5 and HSL. *, nonspecific band. C–E, FA oxidation by cardiomyocytes as assessed by conversion of [¹⁴C]palmitic acid to CO₂ (C), intracellular ASM (D), and extracellular ASM (E). F, total incorporation of FA. Open bar, wild-type mice, and filled bar, Plin5^−/− mice. The assay was performed with or without etomoxir. n = 8–9 representing the number of independent experiments per group. In each experiment, values obtained with three culture dishes were averaged. ***, p < 0.001; **, p < 0.01; ##, p < 0.01; #, p < 0.05, against etomoxir-untreated cells of the same genotype.