Semaphorin3A increases M1-like microglia and retinal ganglion cell apoptosis after optic nerve injury.

ABSTRACT:

Background

The mechanisms leading to retinal ganglion cell (RGC) death after optic nerve injury have not been fully elucidated. Current evidence indicates that microglial activation and M1- and M2-like dynamics may be an important factor in RGC apoptosis after optic nerve crush (ONC). Semaphorin3A (Sema3A) is a classic axonal guidance protein,which has been found to have a role in neuroinflammation processes. In this study, we investigated the contribution of microglial-derived Sema3A to progressive RGC apoptosis through regulating paradigm of M1- and M2-like microglia after ONC.

Method

A mouse ONC model and a primary microglial-RGC co-culture system were used in the present study. The expression of M1- and M2-like microglial activation markers were assessed by real-time pol

SUBMITTER: Yun-Jia L 

PROVIDER: S-EPMC8157735 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature