| The high-mobility group box-1 nuclear factor mediates retinal injury after ischemia reperfusion. | |
| | |
MedLine Citation:
|
PMID: 21828158 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
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. |
| | |
Authors:
|
Galina Dvoriantchikova; Eleut Hernandez; Jeff Grant; Andrea Rachelle C Santos; Huan Yang; Dmitry Ivanov |
Related Documents
:
|
21839778 - The morphology and classification of alpha ganglion cells in the rat retinae: a fractal... 938938 - Differentiation of bergmann glia cells in the cerebellum: a golgi study. 9124808 - Brain regional differences in the expansion of a cag repeat in the spinocerebellar atax... 1793178 - Spatial segregation between populations of ponto-cerebellar neurons: statistical analys... 10477758 - Myosin va movements in normal and dilute-lethal axons provide support for a dual filame... 639088 - The paramedial neurosecretory cells of the suboesophageal ganglion in the cricket, tele... |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-09-09 |
Journal Detail:
|
Title: Investigative ophthalmology & visual science Volume: 52 ISSN: 1552-5783 ISO Abbreviation: Invest. Ophthalmol. Vis. Sci. Publication Date: 2011 |
Date Detail:
|
Created Date: 2011-09-12 Completed Date: 2011-11-04 Revised Date: 2013-01-09 |
Medline Journal Info:
|
Nlm Unique ID: 7703701 Medline TA: Invest Ophthalmol Vis Sci Country: United States |
Other Details:
|
Languages: eng Pagination: 7187-94 Citation Subset: IM |
Affiliation:
|
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Animals, Newborn Antibodies, Neutralizing / pharmacology Blotting, Western Cell Survival Cells, Cultured Coculture Techniques Fluorescent Antibody Technique, Indirect HMGB1 Protein / physiology* Intravitreal Injections Male Mice Mice, Inbred C57BL Mice, Knockout Microscopy, Confocal Neuroglia / pathology Receptors, Immunologic / metabolism Recombinant Proteins / pharmacology Reperfusion Injury / metabolism*, pathology Retinal Diseases / metabolism*, pathology Retinal Ganglion Cells / metabolism*, pathology Reverse Transcriptase Polymerase Chain Reaction Toll-Like Receptor 4 / metabolism |
| Grant Support | |
ID/Acronym/Agency:
|
P30 EY014801/EY/NEI NIH HHS; R21 EY020613-02/EY/NEI NIH HHS; R21EY020613/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Antibodies, Neutralizing; 0/HMGB1 Protein; 0/Receptors, Immunologic; 0/Recombinant Proteins; 0/Tlr4 protein, mouse; 0/Toll-Like Receptor 4; 0/advanced glycosylation end-product receptor |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Choroidal blood flow response to isometric exercise in glaucoma patients and patients with ocular hy...
Next Document: Social support and health in patients with systemic lupus erythematosus (SLE): a literature review.