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Figure 5 | Cardiovascular Diabetology

Figure 5

From: Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β–dependent vascular endothelial cadherin tyrosine phosphorylation

Figure 5

High-concentration glucose induces the phosphorylation of GSKβ (Ser9) and the intracellular accumulation of b-catenin. A, B, Treatment of human umbilical vein endothelial cells (HUVECs) with glucose (10–30 mM, 24 h), LiCl (10 mM, 4 h), or PMA (12.5-50 nM, 4 h) increased phosphorylation of GSK3β (Ser 9). C, Treatment of HUVECs with 50 nM of PMA for 48 h attenuated high-concentration-glucose-induced GSK3β phosphorylation. After treatment of the indicated samples with PMA for 48 h, glucose was added to the indicated samples for 24 h before GSK3β (Ser 9) phosphorylation was evaluated. D, Treatment of HUVECs with 20 mM of glucose for 24 h or 50 nM of PMA for 4 h induced the translocation of β-catenin into the cytoplasm and nuleus of the cells. HUVECs were fixed with 4% paraformaldehyde and stained with primary rabbit polyclonal antibody against β-catenin and secondary FITC-conjugated goat anti-rabbit IgG antibody (green). Hoechst was used to stain the nuclei (blue). Bar = 10 μm. Magnification, 63X. ***P < 0.001, **P < 0.01, and *P < 0.05 vs. control. Each experiment was independently performed 3 to 4 times.

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