Search

Background: Myelin-associated molecules are major impediments to axon regeneration after optic nerve injury. Intravitreal injection of α-crystallin can protect axons from optic nerve degeneration after crushing in rats. Objectives: Our purpose was to investigate whether α-crystallin could counteract the inhibitory effect of myelin and promote neurite growth. Methods: Newborn rat retinal neurons were cultured on myelin-coated dishes with DMEM containing α-crystallin (10-4 g/l) or bovine serum albumin. The density of neurons with neurites and the length of the longest neurite of the cells were analyzed on days 1, 3 and 5. Results: Cultures containing α-crystallin had significantly higher neurite-containing cell densities, and the neurites were significantly longer compared with cultures containing bovine serum albumin. These findings indicated that α-crystallin could counteract the effect of myelin inhibitory factors and stimulate neurite growth. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Purpose: Inhibition of microglial activation has become an important strategy to attenuate neurotoxic damage to the central nervous system. We evaluated the effects of α-crystallin on the production of cytokines in lipopolysaccharides (LPS) and optic nerve injury-activated retinal microglia. Methods: Microglia were collected from retinas of newborn rats, cultured and treated with LPS in vitro. Microglia were also activated by an optic nerve crush in vivo. Pretreatments with and without α-crystallin were performed in cultured cells, and by intravitreal injection in adult rats. Expression of tumor necrosis factor-α (TNF-α), nitric oxide (NO) and inducible NOS synthase (iNOS) were measured by RT-PCR, ELISA, Western blot and the nitrate reductase method. Results: Activated microglia significantly upregulated TNF-α and iNOS mRNA expression and protein production in vitro. An optic nerve crush also increased expression of retinal iNOS and TNF-α protein. Treatment with α-crystallin in vitro and in vivo downregulated their expression. Conclusion: The protective effect of α-crystallin may be due to its effect on microglia via a downregulation in the expression and release of 2 key immune regulatory and inflammatory molecules: TNF-α and iNOS. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

AbstractBackground: RhoA is a small guanosine triphosphatase which participates in signaling pathways of axonal repellents or inhibitors. However, the distribution and expression of RhoA in the rat retina after optic nerve injury has not been elucidated yet. Objectives: To study the distribution and expression of RhoA in the rat retina after optic nerve injury. Methods: Immunohistochemistry was used to determine the distribution of RhoA in rat retina after optic nerve injury. The expression of RhoA was analyzed by Western blot. Results: In normal retina and the retina 1 day after optic nerve injury, RhoA was distributed in the retinal ganglion cell (RGC) layer. Three days after optic nerve injury, it existed in RGCs and the inner plexiform layer. However, 7 days after surgery its immunoreactivity was abundant not only in the RGC and inner plexiform layers but also in the inner nuclear and outer plexiform layers. Western blot analysis showed that the expression of RhoA increased significantly in the retina after optic nerve injury in comparison with normal retina. Conclusion: Theseresults indicate that the distribution and expression of RhoA were extended and enhanced after optic nerve injury, and that RhoA plays an important role in optic nerve regeneration.Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]