Transcriptome analysis reveals dysregulation of genes involved in oxidative phosphorylation in a murine model of retinopathy of prematurity

Transcriptome analysis reveals dysregulation of genes involved in oxidative phosphorylation in a... BackgroundRetinal gene expression pattern is severely altered after exposition to hyperoxia in mice with oxygen-induced retinopathy (OIR), a common model of retinopathy of prematurity. Gene ontology and signaling pathway analyses may add new insights into a better understanding of the pathogenesis of this disease.MethodsSeven-day-old C57BL/6J mice (n = 60) were exposed to 75% oxygen for 5 days and then recovered in room air. The controls (n = 60) were kept in the normoxic conditions. Retinas were harvested immediately following hyperoxia, during the phase of maximal neovascularization, and at the time of neovascularization regression. The retinal RNA samples were evaluated for gene expression using mouse gene expression microarrays. DAVID annotation tools were used for gene ontology and pathway analyses.ResultsThe most significantly enriched signaling pathways during the neovascularization phase of OIR were: focal adhesion; ECM–receptor interaction; PI3K-Akt; oxidative phosphorylation; and Alzheimer’s, Parkinson’s and Huntington’s disease signaling pathways. Genes involved in apoptosis, cell proliferation, cell differentiation, and immune responses were associated with neovascularization regression.ConclusionsPerformed analyses revealed the possible involvement of various signaling pathways in OIR pathomechanism, mostly specific to the OIR phase. Dysregulation of genes involved in oxidative phosphorylation may have an impact on neovascularization development. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pediatric Research Springer Journals

Transcriptome analysis reveals dysregulation of genes involved in oxidative phosphorylation in a murine model of retinopathy of prematurity

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Publisher
Springer Journals
Copyright
Copyright © International Pediatric Research Foundation, Inc 2020
ISSN
0031-3998
eISSN
1530-0447
DOI
10.1038/s41390-020-0793-x
Publisher site
See Article on Publisher Site

Abstract

BackgroundRetinal gene expression pattern is severely altered after exposition to hyperoxia in mice with oxygen-induced retinopathy (OIR), a common model of retinopathy of prematurity. Gene ontology and signaling pathway analyses may add new insights into a better understanding of the pathogenesis of this disease.MethodsSeven-day-old C57BL/6J mice (n = 60) were exposed to 75% oxygen for 5 days and then recovered in room air. The controls (n = 60) were kept in the normoxic conditions. Retinas were harvested immediately following hyperoxia, during the phase of maximal neovascularization, and at the time of neovascularization regression. The retinal RNA samples were evaluated for gene expression using mouse gene expression microarrays. DAVID annotation tools were used for gene ontology and pathway analyses.ResultsThe most significantly enriched signaling pathways during the neovascularization phase of OIR were: focal adhesion; ECM–receptor interaction; PI3K-Akt; oxidative phosphorylation; and Alzheimer’s, Parkinson’s and Huntington’s disease signaling pathways. Genes involved in apoptosis, cell proliferation, cell differentiation, and immune responses were associated with neovascularization regression.ConclusionsPerformed analyses revealed the possible involvement of various signaling pathways in OIR pathomechanism, mostly specific to the OIR phase. Dysregulation of genes involved in oxidative phosphorylation may have an impact on neovascularization development.

Journal

Pediatric ResearchSpringer Journals

Published: Feb 13, 2020

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