Semaphorin 7a regulates inflammatory mediators and permeability in retinal endothelial cells

Abstract

Research supports a key role for inflammation in damaging the retinal vasculature. Current work is designed to investigate regulation of key inflammatory pathways. In this study, we hypothesized that semaphorin 7a (Sema7a) was involved in the increased inflammatory mediators and permeability changes in retinal endothelial cells (REC) grown in high glucose. For these studies, we used diabetic mouse samples and REC to investigate our hypothesis. Primary retinal endothelial cells were grown in normal (5 mM) or high glucose (25 mM glucose) for measurements. In a subset of cells grown in high glucose, cells were transfected with Sema7a siRNA or scrambled siRNA. We measured levels of key inflammatory mediators and zonula occludens-1 (ZO-1) and occludin levels by Western blot. Data suggest that high glucose increased inflammatory mediators and reduced the tight junction proteins, which follows what is often observed in cells grown in high glucose. Sema7a siRNA significantly decreased inflammatory proteins and increased levels of ZO-1 and occludin. These data suggest that Sema7a mediates the actions of high glucose in REC. Use of Sema7a siRNA may offer a new avenue for treatment.