| The relationship of retinal VEGF and retinal IGF-1 mRNA with neovascularization in an acidosis-induced model of retinopathy of prematurity. | |
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MedLine Citation:
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PMID: 16500767 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: Acidosis-induced retinopathy (AIR) in the neonatal rat provides an alternative model for retinopathy of prematurity (ROP). We studied the relationship of vascular endothelial growth factor (VEGF) retinal mRNA and insulin-like growth factor-1 (IGF-1) retinal mRNA expression with the emergence of neovascularization (NV) in AIR. METHODS: Two hundred seventy-five newborn Sprague-Dawley rats were raised in 11 expanded litters of 25. Using our established AIR model, acidosis was induced by twice-daily gavage with NH4Cl from day 2 to day 8 of life (n=175). Rats were sacrificed at days 5, 8, and 10. Nongavaged rats were used as age-matched controls (n=100). Retinae from left eyes were dissected, flatmounts were ADPase-stained, and the presence and severity of NV was scored in a masked manner. Individual right retinae were processed for analysis of retinal VEGF and IGF-1 mRNA using quantitative real-time reverse-transcriptase PCR (qRT-PCR). RESULTS: Retinal VEGF mRNA was increased 1.4-fold at day 10 in AIR, when compared with age-matched controls (p=0.03). This correlated with maximal NV at day 10 in AIR. Retinal IGF-1 mRNA was decreased to 82% of its normal expression on day 8 (p=0.006), prior to maximal NV, before returning to normal expression at day 10, when compared with nonacidotic controls. CONCLUSIONS: In AIR, preretinal neovascularization is associated with decreased retinal IGF-1 mRNA prior to maximal NV and increased retinal VEGF mRNA at the time of maximal NV. These growth factor changes in AIR are similar to those seen with hypercarbic oxygen-induced retinopathy. The retinal IGF-1 pathway may provide an alternative target for therapeutic intervention in abnormal retinal angiogenesis. |
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Authors:
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David A Leske; Jianmin Wu; Martina Mookadam; Yi Chen; Michael P Fautsch; Jonathan M Holmes; William L Lanier |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Current eye research Volume: 31 ISSN: 0271-3683 ISO Abbreviation: Curr. Eye Res. Publication Date: 2006 Feb |
Date Detail:
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Created Date: 2006-02-27 Completed Date: 2006-04-18 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8104312 Medline TA: Curr Eye Res Country: England |
Other Details:
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Languages: eng Pagination: 163-9 Citation Subset: IM |
Affiliation:
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Department of Ophthalmology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis
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chemically induced,
metabolism* Ammonium Chloride / toxicity Animals Animals, Newborn Disease Models, Animal Female Gene Expression Regulation / physiology* Humans Infant, Newborn Insulin-Like Growth Factor I / genetics* Pregnancy RNA, Messenger / metabolism* Rats Rats, Sprague-Dawley Retinal Neovascularization / metabolism* Retinopathy of Prematurity / chemically induced, metabolism* Reverse Transcriptase Polymerase Chain Reaction Vascular Endothelial Growth Factor A / genetics* |
| Grant Support | |
ID/Acronym/Agency:
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EY12798/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; 0/vascular endothelial growth factor A, rat; 12125-02-9/Ammonium Chloride; 67763-96-6/Insulin-Like Growth Factor I |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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