FIGURE 3.
TGF-β1 stimulates metabolic reprogramming via a p38 MAPK pathway. A, IMR-90 cells were treated without or with TGF-β1 (2.5 ng/ml) in the absence or presence of the p38 MAPK inhibitor SB202190 (5 μm) for 48 h at 37 °C. SB202190 was applied 30 min prior to the addition of TGF-β1. Nuclear and cytosolic fractions were then isolated, and the expression levels of phosphorylated PGC-1α (pPGC-1α), lamin A/C, and α-tubulin were determined by Western blotting. B, analysis of total PGC-1α in nuclear fractions in response to TGF-β1 with or without SB202190 treatment. C, IMR-90 cells were treated as described in A. Total and mitochondrial fractions were then isolated. The expression levels of TFAM, VDAC, TOM20, HKII, and α-tubulin were determined by Western blotting. D, bar graph representing the effect of SB202190 (5 μm) on the TGF-β1-induced increase in mitochondrial DNA copy number. Values represent mean ± S.E. Error bars represent S.E. *, p < 0.05 compared with control plus vehicle; #, p < 0.05 compared with TGF-β1 plus vehicle.