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Figure 8 | BMC Neuroscience

Figure 8

From: HIV-1 Tat C phosphorylates VE-cadherin complex and increases human brain microvascular endothelial cell permeability

Figure 8

HIV-1 Tat C mediated tyrosine phosphorylation of VE-cadherin complex and increase in permeability of hBMVECs. HIV-1 Tat C treatment induces the intracellular ROS generation by activating NADPH oxidases (NOX2/NOX4) proteins in hBMVECs. Elevated intracellular levels of ROS activate the levels of redox sensitive kinase PYK2, which led to increased tyrosine phosphorylation of β-catenin and VE-cadherin. HIV-1 Tat C treatment also downregulates major phosphatases VE-PTP and SHP2 and leads to their dissociation from VE-cadherin complex. These shift in PTK/ PTP ratio in hBMVECs after HIV-1 Tat C exposure leads to destabilized junctional assembly and thereby enhanced endothelial permeability.

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