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Updated: Nov 8, 2025
Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
αA-Crystallin inhibits optic nerve astrocyte activation induced by oxygen-glucose deprivation in vitro
Weiyang Shao1, Xiao Liu2, Lixiong Gao1
1Ophthalmology Department, Sixth Medical Center of PLA General Hospital, Beijing 100048, China.
Aims:
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.
Materials And Methods:
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.
Key Findings:
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.
Significance:
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.
