NDLI: Protection of mouse retinal ganglion cell axons and soma from glaucomatous and ischemic injury by cytoplasmic overexpression of Nmnat1.

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Protection of mouse retinal ganglion cell axons and soma from glaucomatous and ischemic injury by cytoplasmic overexpression of Nmnat1.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sasaki, Yo Zhu, Yanli Gidday, Jeffrey M. Zhang, Lihong Milbrandt, Jeffrey
Description	Country affiliation: United States Author Affiliation: Zhu Y ( Department of Neurosurgery, Washington University School of Medicine, St. Louis, MO 63110, USA.)
Abstract	PURPOSE: The Wlds mutation affords protection of retinal ganglion cell (RGC) axons in retinal ischemia and in inducible and hereditary preclinical models of glaucoma. We undertook the present study to determine whether the Nmnat1 portion of the chimeric protein provides axonal and somatic protection of RGCs in models of ischemia and glaucoma, particularly when localized to nonnuclear regions of the cell. METHODS: The survival and integrity of RGC axons and soma from transgenic mice with confirmed cytoplasmic overexpression of Nmnat1 in retina and optic nerve (cytNmnat1-Tg mice) were examined in the retina and postlaminar optic nerve 4 days following acute retinal ischemia, and 3 weeks following the chronic elevation of intraocular pressure. RESULTS: Ischemia- and glaucoma-induced disruptions of proximal segments of RGC axons that comprise the nerve fiber layer in wild-type mice were both robustly abrogated in cytNmnat1-Tg mice. More distal portions of RGC axons within the optic nerve were also protected from glaucomatous disruption in the transgenic mice. In both disease models, Nmnat1 overexpression in extranuclear locations significantly enhanced the survival of RGC soma. CONCLUSIONS: Overexpression of Nmnat1 in the cytoplasm and axons of RGCs robustly protected against both ischemic and glaucomatous loss of RGC axonal integrity, as well as loss of RGC soma. These findings reflect the more pan-cellular protection of CNS neurons that is realized by cytoplasmic Nmnat1 expression, and thus provide a therapeutic strategy for protecting against retinal neurodegeneration, and perhaps other CNS neurodegenerative diseases as well.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.12-10861
Journal	Investigative Opthalmology & Visual Science
Issue Number	1
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-01-02
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Axons Pathology Gene Expression Regulation, Enzymologic Physiology Glaucoma Prevention & Control Nicotinamide-nucleotide Adenylyltransferase Genetics Optic Neuropathy, Ischemic Retinal Diseases Retinal Ganglion Cells Animals Enzymology Cell Survival Cytoplasm Cytoprotection Disease Models, Animal Fluorescent Antibody Technique, Indirect Immunoblotting Mice Mice, Inbred C57bl Mice, Inbred Cba Mice, Transgenic Microscopy, Confocal Optic Nerve Retina 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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