αA-Crystallin inhibits optic nerve astrocyte activation induced by oxygen-glucose deprivation in vitro

A previous study reported that intravitreal injection of αA-crystallin inhibits glial scar formation after optic nerve traumatic injury. The purpose of this study was to investigate the effect of αA-crystallin on optic nerve astrocytes induced by oxygen glucose deprivation (OGD) in vitro. Optic nerve astrocytes from newborn Long Evans rats were cultured with αA-crystallin (10−4 g/l) to detect the effects of αA-crystallin on astrocytes. Using a scratch assay, the effect of αA-crystallin treatment on astrocyte migration was assessed. Astrocytes were exposed to OGD and glucose reintroduction/reoxygenation culture for 24 h and 48 h. The expression of glial fibrillary acidic protein (GFAP) and neurocan were subsequently evaluated via immunocytochemistry and western blot. BMP2/4, BMPRIa/Ib and Smad1/5/8 mRNA expression levels were detected by RT-PCR. The results showed that αA-crystallin slowed the migration of astrocytes in filling the scratch gaps. GFAP and neurocan expression in astrocytes was increased after OGD. However, after treatment with αA-crystallin, GFAP and neurocan expression levels clearly decreased. Furthermore, RT-PCR showed that BMP2 and BMP4 mRNA expression levels decreased significantly. These results suggest that αA-crystallin inhibits the activation of astrocytes after OGD injury in vitro. Inhibition of the BMP/Smad signaling pathway might be the mechanism underlying this effect. •We observed the inhibition of αA-crystallin in astrocyte activation in vitro.•αA-crystallin inhibited the migration of astrocytes in scratch assay.•αA-crystallin inhibited astrocyte GFAP and neurocan expression after oxygen glucose deprivation.•αA-crystallin inhibited astrocyte BMPs mRNA expression after oxygen glucose deprivation.