NDLI: The High-Mobility Group Box-1 Nuclear Factor Mediates Retinal Injury after Ischemia Reperfusion

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The High-Mobility Group Box-1 Nuclear Factor Mediates Retinal Injury after Ischemia Reperfusion

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The High-Mobility Group Box-1 Nuclear Factor Mediates Retinal Injury after Ischemia Reperfusion

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hernandez, Eleut Ivanov, Dmitry Santos, Andrea Rachelle C. Yang, Huan Grant, Jeff Dvoriantchikova, Galina
Description	Country affiliation: United States Author Affiliation: Dvoriantchikova G ( Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.)
Abstract	PURPOSE: High-mobility group protein B1 (Hmgb1) is released from necrotic cells and induces an inflammatory response. Although Hmgb1 has been implicated in ischemia/reperfusion (IR) injury of the brain, its role in IR injury of the retina remains unclear. Here, the authors provide evidence that Hmgb1 contributes to retinal damage after IR. METHODS: Retinal IR injury was induced by unilateral elevation of intraocular pressure and the level of Hmgb1 in vitreous humor was analyzed 24 hours after reperfusion. To test the functional significance of Hmgb1 release, ischemic or normal retinas were treated with the neutralizing anti-Hmgb1 antibody or recombinant Hmgb1 protein respectively. To elucidate in which cell type Hmgb1 exerts its effect, primary retinal ganglion cell (RGC) cultures and glia RGC cocultures were treated with Hmgb1. To clarify the downstream signaling pathways involved in Hmgb1-induced effects in the ischemic retina, receptor for advanced glycation end products (Rage)-deficient mice (RageKO) were used. RESULTS: Hmgb1 is accumulated in the vitreous humor 24 hours after IR. Inhibition of Hmgb1 activity with neutralizing antibody significantly decreased retinal damage after IR, whereas treatment of retinas or retinal cells with Hmgb1 induced a loss of RGCs. The analysis of RageKO versus wild-type mice showed significantly reduced expression of proinflammatory genes 24 hours after reperfusion and significantly increased survival of ganglion cell layer neurons 7 days after IR injury. CONCLUSIONS: These results suggest that an increased level of Hmgb1 and signaling via the Rage contribute to neurotoxicity after retinal IR injury.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.11-7793
Journal	Investigative Opthalmology & Visual Science
Issue Number	10
Volume Number	52
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2011-09-09
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Hmgb1 Protein Physiology Reperfusion Injury Metabolism Retinal Diseases Retinal Ganglion Cells Advanced Glycosylation End Product-specific Receptor Animals Animals, Newborn Antibodies, Neutralizing Pharmacology Blotting, Western Cell Survival Cells, Cultured Coculture Techniques Fluorescent Antibody Technique, Indirect Intravitreal Injections Mice Mice, Inbred C57bl Mice, Knockout Microscopy, Confocal Neuroglia Pathology Receptors, Immunologic Recombinant Proteins Reverse Transcriptase Polymerase Chain Reaction Toll-like Receptor 4 Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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