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SL Bernstein, M Mintz, D Stephan, Y Guo; Gene Expression Changes During Early Anterior Ischemic Optic Neuropathy (AION) . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3924.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:Anterior ischemic optic neuropathy (AION) is an ischemic optic neuropathy causing retinal ganglion cell (RGC) death and vision loss in a large number of patients. We recently described a new rodent model of AION (Bernstein et al, 2001). Our preliminary work has determined that RGC function alters within one day, and reactive retinal changes may occur by three days. We wanted to identify the large scale changes in gene expression occurring from AION, and identify genes with retinal ganglion cell (RGC) -intensive functions. Methods:All animal procedures were performed using IACUC-approved protocols. AION was induced in 6 male Sprague-Dawley albino rats as previously described. One eye was treated in each animal to produce AION, and the second eye utilized as an internal control. Two time points were utilized: (R1) 1 day (RGC-specific/early) and (R3) 3 days (retina reactive/late). Total retina RNA was isolated and pooled from experimental and control eyes from both time points. Biotinylated cDNA probes were prepared, and reacted with Affymetrix U34A rat total gene expression arrays (∼10,000 genes/chip). Expression analysis was compared between control eyes (early and late) and experimental eyes (early and late), as well as between control and experimental eyes in each period. Changes ≷2.0 fold between groups were considered to be significant. Results:2228 genes were identified in the retinae of all eyes. Approximately 100 ESTs increased separately in either the R1 or R3 periods, compared to control. Fewer (∼20) ESTs increased at both times. Similar numbers were seen to decline in each group from R1 and R3 periods, with a subset (N=12) of ESTs decreasing in both groups. Some of these ESTs correspond to genes differentially expressed in the human fovea, and likely correspond to RGC-enriched or differentially expressed genes. Conclusion:AION in rodents alters expression of an identifiable subset of genes likely to be directly involved in RGC function, and the retinal response to RGC distress. Identification of these specific genes suggests potential pathways by which AION in humans may be amenable to treatment.
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