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Objective: To investigate the effects and mechanism of tyrosine kinase receptor B (TrkB) on the vascular endothelial permeability. Methods: The counts of FITC-labeled dextran and T cells which were entered through the endothelial monolayer into the lower chamber were detected by Transwell chamber. The TrkB gene and VEcadherin gene were cloned into a vector, which was transfected into 293T cells. The expressions of VEcadherin mRNA and Est1 were detected by real-time PCR, and the expressions of VE-cadherin protein were detected by Western blot. Results: TrkB knockdown could significantly increase the FITC-labeled dextran diffusion, VE-cadherin gap formation and migration of T cells across the endothelial monolayer. Meanwhile, TrkB knockdown also decreased the expressions of VE-cadherin mRNA and protein. Importantly, he FITC-labeled dextran diffusion, VE-cadherin gap formation and migration of T cells regulated by TrkB knockdown were all prevented by overexpressing VE-cadherin. Besides, TrkB knockdown also decreased the expression of Est1. The results above were different of the control group, P<0.05. Conclusion: There are significant evidences that TrkB could protect the vascular endothelial permeability by regulating the synthesis of VE-cadherin and inhibiting the degradation of VE-cadherin.

biomedical research/biomedical research

The study of TrkB pathway on vascular endothelial permeability by regulating the synthesis of VE-cadherin and inhibiting the degradation of VE-cadherin