Abstract:
AIM:To explore the effects of αA-crystallin in astrocyte gliosis after optic nerve crush (ONC) and the mechanism of α-crystallin in neuroprotection and axon regeneration. METHODS:ONC was established on the Sprague-Dawley rat model and αA-crystallin (10(-4) g/L, 4 µL) was intravitreously injected into the rat model. Flash-visual evoked potential (F-VEP) was examined 14d after ONC, and the glial fibrillary acidic protein (GFAP) levels in the retina and crush site were analyzed 1, 3, 5, 7 and 14d after ONC by immunohistochemistry (IHC) and Western blot respectively. The levels of beta Tubulin (TUJ1), growth-associated membrane phosphoprotein-43 (GAP-43), chondroitin sulfate proteoglycans (CSPGs) and neurocan were also determined by IHC 14d after ONC. RESULTS:GFAP level in the retina and the optic nerve significantly increased 1d after ONC, and reached the peak level 7d post-ONC. Injection of αA-crystallin significantly decreased GFAP level in both the retina and the crush site 3d after ONC, and induced astrocytes architecture remodeling at the crush site. Quantification of retinal ganglion cell (RGC) axons indicated αA-crystallin markedly promoted axon regeneration in ONC rats and enhanced the regenerated axons penetrated into the glial scar. CSPGs and neurocan expression also decreased 14d after αA-crystallin injection. The amplitude (N1-P1) and latency (P1) of F-VEP were also restored. CONCLUSION:Our results suggest α-crystallin promotes the axon regeneration of RGCs and suppresses the activation of astrocytes.
journal_name
Int J Ophthalmoljournal_title
International journal of ophthalmologyauthors
Shao WY,Liu X,Gu XL,Ying X,Wu N,Xu HW,Wang Ydoi
10.18240/ijo.2016.07.04subject
Has Abstractpub_date
2016-07-18 00:00:00pages
955-66issue
7eissn
2222-3959issn
2227-4898pii
ijo-09-07-955journal_volume
9pub_type
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