NDLI: Inhibition of histone deacetylase protects the retina from ischemic injury.

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Inhibition of histone deacetylase protects the retina from ischemic injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Husain, Shahid Menick, Donald R. Crosson, Craig E. Alsarraf, Oday Mani, Santhosh K.
Description	Country affiliation: United States Author Affiliation: Crosson CE ( Department of Ophthalmology, Storm Eye Institute, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina, USA. crossonc@musc.edu)
Abstract	PURPOSE. The pathogenesis of retinal ischemia results from a series of events involving changes in gene expression and inflammatory cytokines. Protein acetylation is an essential mechanism in regulating transcriptional and inflammatory events. The purpose of this study was to investigate the neuroprotective action of the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) in a retinal ischemic model. METHODS. To investigate whether HDAC inhibition can reduce ischemic injury, rats were treated with TSA (2.5 mg/kg intraperitoneally) twice daily on days 0, 1, 2, and 3. Seven days after ischemic injury, morphometric and electroretinographic (ERG) analyses were used to assess retinal structure and function. Western blot and immunohistochemical analyses were used to evaluate TSA-induced changes in histone-H3 acetylation and MMP secretion. RESULTS. In vehicle-treated animals, ERG a- and b-waves from ischemic eyes were significantly reduced compared with contralateral responses. In addition, histologic examination of these eyes revealed significant degeneration of inner retinal layers. In rats treated with TSA, amplitudes of ERG a- and b-waves from ischemic eyes were significantly increased, and normal inner retina morphology was preserved. Ischemia also increased the levels of retinal TNF-alpha, which was blocked by TSA treatment. In astrocyte cultures, the addition of TNF-alpha (10 ng/mL) stimulated the secretion of MMP-1 and MMP-3, which were blocked by TSA (100 nM). CONCLUSIONS. These studies provide the first evidence that suppressing HDAC activity can protect the retina from ischemic injury. This neuroprotective response is associated with the suppression of retinal TNF-alpha expression and signaling. The use of HDAC inhibitors may provide a novel treatment for ischemic retinal injury.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.09-4538
Journal	Investigative Opthalmology & Visual Science
Issue Number	7
Volume Number	51
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2010-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Histone Deacetylase Inhibitors Pharmacology Histone Deacetylases Metabolism Hydroxamic Acids Reperfusion Injury Prevention & Control Retina Drug Effects Retinal Diseases Acetylation Animals Blotting, Western Electroretinography Histones Immunohistochemistry Matrix Metalloproteinase 1 Matrix Metalloproteinase 3 Neuroprotective Agents Rats, Inbred Bn Enzymology Tumor Necrosis Factor-alpha 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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