Figure 7 | Laboratory Investigation

Figure 7

From: Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF

Figure 7The alternative text for this image may have been generated using AI.

(a–f) Role of GLUT1 in VEGF-induced MC FN production. (a) Primary culture mouse MCs with the C57BL6 background were studied in culture with and without VEGF-A165 peptide (2 ng/ml) for 48 h. VEGF-A165 stimulated a two-fold increase in MC GLUT1 protein. (b) Graph of western blot data from MCs treated with VEGF. **P<0.05, n=4 in each group). (c) Graph of 3H2-deoxyglucose (DOG) uptake rates in cultured MCs treated with or without VEGF-A165 2 ng/ml for 48 h, **P<0.05 for VEGF-A165-treated cells vs controls, n=4 samples per group. The glucose uptake rate increased 3.6-fold in response to treatment with VEGF-A165. (d) FN protein increased 3.3-fold in response to the VEGF-A165 treatment, n=3 in each group. (e) In comparison, FN increased only 1.6-fold in cultured MCs from antisense-GLUT1 transgenic mice in response to the 2 ng/ml VEGF-A165 treatment for 48 h. (f) Graph of western blot data from MCs isolated from normal and antisense-GLUT1 transgenic mice, treated with VEGF. *P<0.01 and **P<0.05 vs controls.

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