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Figure 4 | Cardiovascular Diabetology

Figure 4

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

Figure 4

Phosphorylation of myosin light chain (MLC) mediates high-concentration glucose-induced tyrosine phosphorylation of VE-cad. A, Treatment of human umbilical vein endothelial cells (HUVECs) with glucose for 24 h led to phosphorylation of MLC and MLC phosphatase regulatory subunit (MYPT). B, High-concentration glucose-induced VE-cad tyrosine phosphorylation was attenuated in HUVECs overexpressing mutant MLC (AA-MLC), in which Thr18 and Ser19 are replaced with alanines. HUVECs were transfected with the indicated constructs and, after 48 h, were treated with 20 mM glucose for 24 h. C, Cytochalasin D suppressed high- concentration glucose-induced tyrosine phosphorylation of VE-cad. HUVECs were treated with 20 mM glucose for 24 h and then 1 μM cytochalasin D for 2 h. D, Treatment of HUVECs with protein kinase A inhibitor H89 for 2 h led to tyrosine phosphorylation of VE-cad. E, Treatment of HUVECs with 10 μM forskolin for 2 h (an activator of adenylate cyclase) attenuated high-concentration-induced tyrosine phosphorylation of VE-cad. HUVECs were first treated with 20 mM of glucose for 24 h. *P < 0.05, ***P < 0.001 vs. control. Each experiment was independently performed 3 to 4 times.

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