Skip to main content
. 2022 Mar 8;7(5):e155260. doi: 10.1172/jci.insight.155260

Figure 6. PPKM2Tg regulated VEGF production in the regulation of mitochondrial function in glomeruli.

Figure 6

Glomeruli from WT and PPKM2Tg mice were incubated with anti-VEGF(1 μg/mL) for 24 hours, and a Seahorse assay was performed. (A–D) Representative curve of OCR (A) and ECAR (C), as well as quantitated data (B and D), were shown. For OCR, WT (n = 16); WT + anti-VEGF (n = 7); Tg (n = 9); Tg + anti-VEGF (n = 7). *P < 0.05. For ECAR, WT (n = 8); WT + anti-VEGF (n = 8); Tg (n = 12); Tg + anti-VEGF (n = 7). *P < 0.05. Data are mean ± SEM, 2-way ANOVA followed by correction for multiple comparisons with Tukey’s post hoc test. Glomeruli from diabetic PPKM2Tg mice were treated with anti-VEGF (10 μg/mL) for 24 hours. (E and F) Representative curve of OCR and quantitated data were shown in E and F. Tg 7MSTZ (n = 13); Tg 7MSTZ + anti-VEGF (n = 11). *P < 0.05. Diabetic WT mice 7–9 months after STZ (7-9MSTZ) were incubated with mVEGF (100 ng/mL) for 24 hours and addition of mVEGF (100 ng/mL) 1 hour before Seahorse assay. (G and H) Representative curve of OCR and quantitated data. WT 7-9MSTZ (n = 10); WT 7-9MSTZ + VEGF 24/1h (n = 9). *P < 0.05. Data are mean ± SEM.