Dexamethasone intensify the tight junctions in rat retinal vascular endothelial cells in vitro

Abstract

To investigate the effect of dexamethasone on the expression, distribution and function of tight junctions in rat retinal vascular endothelial cells in vitro. Try to explain the mechanism of glucocorticoid in the treatment of macular edema from a new viewpoint. Rat retinal vascular endothelial cells were isolated and purified by magnetic beads coated with anti-CD31. Cells were identified by vW factor indirect immunofluorescence staining. The fourth-passage cells were used to investigate the effect of dexamethasone on the tight junctions in rat retinal vascular endothelial cells. Cells were separated into two groups, one was treated with 500 nmol/L dexamethasone and the other was used as the control. Transepithelial electrical resistance (TER) was measured to estimate the changes in the treated group. Indirect immunofluorescent stain and RT-PCR were used to observe the difference of tight junction protein distribution and mRNA expression level between these two groups. Rat retinal vascular endothelial cell monolayer showed positive immunofluorescent staining for vW factor. The dexamethasone treated group showed greater TER than that of the control (P < 0.01). Tight junction protein in the dexamethasone treated group localized closer to the borders of retinal vascular endothelial cells than that of the control. Claudin-1 mRNA level of the dexamethasone treated cells were greater than that of the control. Dexamethasone intensifies the tight junctions in rat retinal vascular endothelial cells. Therefore this is one of the mechanisms of treatment of macular edema by glucocorticoid.