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. 2022 Jan 13;42(3):326–342. doi: 10.1161/ATVBAHA.121.317093

Figure 7.

Figure 7.

HIF1A-GLUT1 pathway was upregulated in microRNA-126 (miR-126)–deficient endothelial cells (ECs), and miR-126-3p agomir restored the disrupted glycometabolism in miR-126 knocked out mice. A, Dual immunofluorescence of GLUT1 (glucose transporter 1) and PECAM1 (platelet endothelial cell adhesion molecule-1) in miR-126–deficient and littermate control hepatic tissues at embryos at day 14.5 (E14.5). Scale bar=100 µm. B, Dual immunofluorescence of HIF1A (hypoxia-inducible factor 1-alpha) and PECAM1 in miR-126–deficient and littermate control hepatic tissues at E14.5. Scale bar=100 µm. C, Western Blotting of glucose transport protein family (GLUT1, GLUT2 and GLUT3) and HIF1A in adult miR-126–deficient and wild-type hepatic ECs. D, Quantification of immunoblotting results in C. E, Intraperitoneal glucose tolerance test (IGTT) on wild types, miR-126–deficient mice treated with miR-126-3p agomir, agomir-negative control (NC) and no treats. Sample size: n=6. F, Area under curves (AUC) analysis IGTT results. Sample size: n=6. PIK3R2 indicates phosphoinositide-3-kinase regulatory subunit 2; and SLC2A, solute carrier family 2.