Fig. 5: The reduction of oxidative phosphorylation and glycolysis by a NOX4 inhibitor in TGF-β1-induced HPMCs. | Cell Death & Disease

Fig. 5: The reduction of oxidative phosphorylation and glycolysis by a NOX4 inhibitor in TGF-β1-induced HPMCs.

From: Autophagy caused by oxidative stress promotes TGF-β1-induced epithelial-to-mesenchymal transition in human peritoneal mesothelial cells

Fig. 5

A The determination of ROS production using DCF-DA (n = 4). B Mitochondrial superoxide production in live cells was measured using fluorescence microscopy with MitoSOX Red dye. Representative fluorescence images showing the localization of MitoSOX Red fluorescence. Scale bar = 40 μm. C, D The level of MitoSOX Red fluorescence per cell was quantified using ImageJ software. Image data from 51–60 cells per treatment condition were averaged (n = 3). E, F The measurement of mitochondrial oxygen consumption ratio (OCR) and extracellular acidification rates (ECAR) under NOX4 inhibition with GKT137831-treated HPMCs. The parametric indices of OCR and ECAR, mitochondrial respiration, and glycolysis are shown (n = 4–6). G, H The measurement of mitochondrial OCR and extracellular acidification rates (ECAR) under autophagy inhibition by 3-MA treatment. The parametric indices of OCR and ECAR, mitochondrial respiration, and glycolysis are shown. (n = 4–7). The data are presented as mean ± standard error (SE). *P < 0.05 vs. control, ***P < 0.001 vs. control; #P < 0.05 vs. TGF-β1 2 ng/mL; ##P < 0.01 vs. TGF-β1 2 ng/mL; ###P < 0.001 vs. TGF-β1 2 ng/mL; +P < 0.05 vs. TGF-β1 5 ng/mL; ++P < 0.01 vs. TGF-β1 5 ng/mL; and +++P < 0.001 vs. TGF-β1 5 ng/mL.

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