Figure 3

PEDF and 44mer regulate TG degradation in cardiomyocytes. A: western blot determination for PEDF protein expression in a rat AMI model. B: densitometry of the western blots shown in (A), normalized to β-actin. n = 3, values are means ± SD. *P < 0.05 compared with normal group. **P < 0.05 compared with normal group and PEDF group. C: intracellular lipids were stained with oil Red O 4 weeks after AMI. The siPEDF group showed an abundance of lipid droplets, whereas the PEDF group showed very little staining. Scale bar, 40 μm. D: quantification of the lipid content in the heart on 4 weeks after AMI by biochemical methods. n = 3, values are means ± SD. *P < 0.05 compared with normal group; **P < 0.05 compared with vector group. #P < 0.05 compared with vector group and siPEDF group. E: the intracellular lipids were stained with oil Red O after 1 day of hypoxia. The hypoxia group showed an abundance of lipid droplets, whereas the rPEDF (10 nM) and 44mer (10 nM) groups showed very little staining. Scale bar, 20 μm. F: quantification of lipid content in cardiomyocytes after 1 day of hypoxia by biochemical methods. n = 3, values are means ± SD. *P < 0.05 compared with normal group; #P < 0.05 compared with hypoxia group. G: Influence of PEDF and 44mer on intracellular FFA under hypoxia condition. Values are means ± SD. *P < 0.05 compared with hypoxia group. H: PEDF downregulation in cardiomyocytes significantly increased the TG content compared to wild-type cardiomyocytes. The TG content did not significantly change in WT cardiomyocytes treated with rPEDF or 44mer, while the addition of rPEDF or 44mer to cardiomyocytes that expressed less PEDF significantly decreased the TG content. n = 3, values are means ± SD. *P < 0.05 compared with control group; #P < 0.05 compared with siPEDF group.