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Approaches to Potentiated Neuroprotective Treatment in the Rodent Model of Ischemic Optic Neuropathy
UMB Dataset

UID: 206

Author(s): Zara Mehrabian, Yan Guo, Neil R. Miller, Amanda D. Henderson, Steven Roth, Steven L. Bernstein* * Corresponding Author
Nonarthritic anterior ischemic optic neuropathy (NAION) commonly causes sudden optic nerve (ON)-related vision loss. The rodent NAION model (rAION) closely resembles NAION in presentation and physiological responses. Researchers hypothesized that blocking pro-inflammatory prostaglandin (PGE2) production by inhibiting monoacylglycerol lipase or cyclooxygenase activity and co-administering PGJ2 would potentiate RGC survival following ischemic neuropathy. This study identified early rAION-associated optic nerve head (ONH) inflammatory gene expression responses and the anti-inflammatory prostaglandin PGJ2’s effects on those responses. Deep sequencing was performed on vehicle- and PGJ2-treated ONHs 3d post-rAION induction. Results were compared against responses from a retinal ischemia model. Animals were treated with PGJ2 and MAGL inhibitor KML29, or PGJ2 + COX inhibitor meloxicam. RGC survival was quantified by stereology.
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Data Type
Equipment Used
BioAnalyzer 2100
Heidelberg SD-OCT
Nikon E800
Oculight GLx
planoconver contact lens
rat fundus contact lens
Varioskan LUX microplate reader
warming pads
Software Used
Ingenuity pathway analysis software
Stereo Investigator 10
Study Type
Dataset Format(s)
Microsoft Excel
Dataset Size
Grant Support
RO1EY015304/National Eye Institute
R21EY028690/National Eye Institute