Fig. 6.

Effect of downregulated CPT1A on mitochondrial metabolism in senescent PD-MSCs. a To analyzed mitochondrial function of PD-MSCs with CPT1A siRNA, the mitochondrial mass, b the ROS levels, c mitochondrial membrane potential, and d ATP production were analyzed in late passage PD-MSCs treated with CPT1A siRNA such as CPT1A inhibitor compared to control. The glycolytic ability of senescent PD-MSCs treated with etomoxir such as CPT1A inhibitor was determined by XF24 analyzer. e The extracellular acidification rate (ECAR) of early and late passage PD-MSCs was analyzed by using glycolysis-XF assay kit and f also determined in late passage PD-MSCs treated with etomoxir. g The mitochondrial oxygen consumption rate (OCR) of early and late passage was determined by using mitochondrial stress-XF assay kit and h also determined after the treatment with etomoxir. i The oxygen consumption rates (OCR) of fatty acid, glucose, and glutamine pathways were analyzed in early passage PD-MSCs and j late passage PD-MSCs treated with siRNA and etomoxir. The data were representative of three independent experiments and expressed as means ± S.D. An asterisk indicates P < 0.05 versus early passage. Red, early; blue, late; pink, hTERT+. Red, control; blue, etomoxir; pink, CPT1A siRNA