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Gene expression microarray analysis of early oxygen-induced retinopathy in the rat.

Tea M, Fogarty R, Brereton HM, Michael MZ, Van der Hoek MB, Tsykin A, Coster DJ, Williams KA - J Ocul Biol Dis Infor (2009)

Bottom Line: Quantitative real-time RT-PCR analysis of Egln3, Bnip3, Slc16a3, and Hk2 confirmed the microarray results.We conclude that combined methodologies are required for adequate dissection of the pathophysiology of strain susceptibility to OIR in the rat.ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12177-009-9041-7) contains supplementary material, which is available to authorized users.

View Article: PubMed Central - PubMed

ABSTRACT
Different inbred strains of rat differ in their susceptibility to oxygen-induced retinopathy (OIR), an animal model of human retinopathy of prematurity. We examined gene expression in Sprague-Dawley (susceptible) and Fischer 344 (resistant) neonatal rats after 3 days exposure to cyclic hyperoxia or room air, using Affymetrix rat Genearrays. False discovery rate analysis was used to identify differentially regulated genes. Such genes were then ranked by fold change and submitted to the online database, DAVID. The Sprague-Dawley list returned the term "response to hypoxia," absent from the Fischer 344 output. Manual analysis indicated that many genes known to be upregulated by hypoxia-inducible factor-1alpha were downregulated by cyclic hyperoxia. Quantitative real-time RT-PCR analysis of Egln3, Bnip3, Slc16a3, and Hk2 confirmed the microarray results. We conclude that combined methodologies are required for adequate dissection of the pathophysiology of strain susceptibility to OIR in the rat. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12177-009-9041-7) contains supplementary material, which is available to authorized users.

No MeSH data available.


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Montages of representative sectors of retinae of room air-exposed and cyclic hyperoxia-exposed rats collected at post-natal day 3 and stained with fluorochrome-conjugated GS-IB4 to highlight the vasculature. a F344 rat raised in room air; b F344 rat exposed to cyclic hyperoxia from birth; c SD rat raised in room air; d SD rat exposed to cyclic hyperoxia from birth
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Fig1: Montages of representative sectors of retinae of room air-exposed and cyclic hyperoxia-exposed rats collected at post-natal day 3 and stained with fluorochrome-conjugated GS-IB4 to highlight the vasculature. a F344 rat raised in room air; b F344 rat exposed to cyclic hyperoxia from birth; c SD rat raised in room air; d SD rat exposed to cyclic hyperoxia from birth

Mentions: Montages of representative sectors from the retinae of 3-day-old F344 and SD rats exposed to cyclic hyperoxia from birth or raised in room air are shown in Fig. 1. During normal retinal vascular development, vessels develop from the optic nerve head (indicated by arrow) towards the peripheral retina. At post-natal day 3, vessels in the room air-exposed and cyclic hyperoxia-exposed F344 rats, and in the room air-exposed SD rats, had begun to develop and showed normal morphology (Fig. 1a–c). SD rats exposed to cyclic hyperoxia showed aberrant vascular development, with fewer vessels radiating from the optic nerve head and reduced density of the capillary network (Fig. 1d).Fig. 1


Gene expression microarray analysis of early oxygen-induced retinopathy in the rat.

Tea M, Fogarty R, Brereton HM, Michael MZ, Van der Hoek MB, Tsykin A, Coster DJ, Williams KA - J Ocul Biol Dis Infor (2009)

Montages of representative sectors of retinae of room air-exposed and cyclic hyperoxia-exposed rats collected at post-natal day 3 and stained with fluorochrome-conjugated GS-IB4 to highlight the vasculature. a F344 rat raised in room air; b F344 rat exposed to cyclic hyperoxia from birth; c SD rat raised in room air; d SD rat exposed to cyclic hyperoxia from birth
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2821581&req=5

Fig1: Montages of representative sectors of retinae of room air-exposed and cyclic hyperoxia-exposed rats collected at post-natal day 3 and stained with fluorochrome-conjugated GS-IB4 to highlight the vasculature. a F344 rat raised in room air; b F344 rat exposed to cyclic hyperoxia from birth; c SD rat raised in room air; d SD rat exposed to cyclic hyperoxia from birth
Mentions: Montages of representative sectors from the retinae of 3-day-old F344 and SD rats exposed to cyclic hyperoxia from birth or raised in room air are shown in Fig. 1. During normal retinal vascular development, vessels develop from the optic nerve head (indicated by arrow) towards the peripheral retina. At post-natal day 3, vessels in the room air-exposed and cyclic hyperoxia-exposed F344 rats, and in the room air-exposed SD rats, had begun to develop and showed normal morphology (Fig. 1a–c). SD rats exposed to cyclic hyperoxia showed aberrant vascular development, with fewer vessels radiating from the optic nerve head and reduced density of the capillary network (Fig. 1d).Fig. 1

Bottom Line: Quantitative real-time RT-PCR analysis of Egln3, Bnip3, Slc16a3, and Hk2 confirmed the microarray results.We conclude that combined methodologies are required for adequate dissection of the pathophysiology of strain susceptibility to OIR in the rat.ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12177-009-9041-7) contains supplementary material, which is available to authorized users.

View Article: PubMed Central - PubMed

ABSTRACT
Different inbred strains of rat differ in their susceptibility to oxygen-induced retinopathy (OIR), an animal model of human retinopathy of prematurity. We examined gene expression in Sprague-Dawley (susceptible) and Fischer 344 (resistant) neonatal rats after 3 days exposure to cyclic hyperoxia or room air, using Affymetrix rat Genearrays. False discovery rate analysis was used to identify differentially regulated genes. Such genes were then ranked by fold change and submitted to the online database, DAVID. The Sprague-Dawley list returned the term "response to hypoxia," absent from the Fischer 344 output. Manual analysis indicated that many genes known to be upregulated by hypoxia-inducible factor-1alpha were downregulated by cyclic hyperoxia. Quantitative real-time RT-PCR analysis of Egln3, Bnip3, Slc16a3, and Hk2 confirmed the microarray results. We conclude that combined methodologies are required for adequate dissection of the pathophysiology of strain susceptibility to OIR in the rat. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12177-009-9041-7) contains supplementary material, which is available to authorized users.

No MeSH data available.


Related in: MedlinePlus