Expression variation in the mouse retina
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE24512 | GEO | 2012/03/15
SECONDARY ACCESSION(S): PRJNA132589
REPOSITORIES: GEO
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Project description:Expression analysis of multiple mouse strains across two developmental timepoints to determine both strain specific and temporal expression of genes in the mouse retina A total of 29 retinas were collected from 15 mice of each strain at similar time points during the day. Equimolar amounts of RNA isolated from ten retinas were pooled into three separate pools from each strain and time point, then hybridized to Affymetrix Mouse 420A 2.0 GeneChip arrays.
2012-03-15 | E-GEOD-24512 | biostudies-arrayexpress
Project description:PURPOSE: Hyperoxia is toxic to photoreceptors, and this toxicity may be important in the progress of retinal dystrophies. This microarray study examines gene expression induced in the C57BL/6J mouse retina by hyperoxia over the 14-day period during which photoreceptors first resist, then succumb to, hyperoxia. METHODS: Young adult C57BL/6J mice were exposed to hyperoxia (75% oxygen) for up to 14 days. On day 0 (control), day 3, day 7, and day 14, retinal RNA was extracted and processed on Affymetrix GeneChip Mouse Genome 430 2.0 arrays. Microarray data were analyzed using GCOS Version 1.4 and GeneSpring Version 7.3.1. RESULTS: The overall numbers of hyperoxia-regulated genes increased monotonically with exposure. Within that increase, however, a distinctive temporal pattern was apparent. At 3 days exposure, there was prominent upregulation of genes associated with neuroprotection. By day 14, these early-responsive genes were downregulated, and genes related to cell death were strongly expressed. At day 7, the regulation of these genes was mixed, indicating a possible transition period from stability at day 3 to degeneration at day 14. CONCLUSIONS: Microarray analysis of the response of the retina to prolonged hyperoxia demonstrated a temporal pattern involving early neuroprotection and later cell death, and provided insight into the mechanisms involved in the two phases of response. As hyperoxia is a consistent feature of the late stages of photoreceptor degenerations, understanding the mechanisms of oxygen toxicity may be important therapeutically. 4 timepoints in total, 0d (control), 3d, 7d and 14d and a replicate per timepoint. Total of 8 chips.
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