NDLI: MicroRNA-200b downregulates oxidation resistance 1 (Oxr1) expression in the retina of type 1 diabetes model.

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MicroRNA-200b downregulates oxidation resistance 1 (Oxr1) expression in the retina of type 1 diabetes model.

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MicroRNA-200b downregulates oxidation resistance 1 (Oxr1) expression in the retina of type 1 diabetes model.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Murray, Anne R. Zhou, Kevin K. Park, Kyoungmin Takahashi, Yusuke Chen, Qian Ma, Jian-xing
Description	Country affiliation: United States Author Affiliation: Murray AR ( Department of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Boulevard, Oklahoma City, OK 73104, USA.)
Abstract	PURPOSE: MicroRNAs (miRNAs) are known to participate in post-transcriptional regulation of gene expression and are involved in multiple pathogenic processes. Here, we identified miRNA expression changes in the retinas of Akita mice, a genetic model of type 1 diabetes, and investigated the potential role of miRNA in diabetic retinopathy. METHODS: Visual function of Akita and control mice was evaluated by electroretinography. MiRNA expression changes in the retinas of Akita mice were identified by miRNA-specific microarray and confirmed by quantitative RT-PCR (qRT-PCR). The potential downstream targets of identified miRNAs were predicted by bioinformatic analysis using web-based applications and confirmed by dual luciferase assay. The mRNA and protein changes of identified downstream targets were examined by qRT-PCR and Western blot analysis. RESULTS: MiRNA-specific microarray and qRT-PCR showed that miR-200b was upregulated significantly in the Akita mouse retina. Sequence analysis and luciferase assay identified oxidation resistance 1 (Oxr1) as a downstream target gene regulated by miR-200b. In a human Müller cell line, MIO-M1, transfection of a miR-200b mimic downregulated Oxr1 expression. Conversely, transfection of MIO-M1 with a miR-200b inhibitor resulted in upregulated Oxr1. Furthermore, overexpression of recombinant Oxr1 attenuated oxidative stress marker, nitration of cellular proteins, and ameliorated apoptosis induced by 4-hydroxynonenal (4-HNE), an oxidative stressor. Similarly, transfection of a miR-200b inhibitor decreased, whereas transfection of miR-200b mimic increased the number of apoptotic cells following 4-HNE treatment. CONCLUSIONS: These results suggested that miR-200b-regulated Oxr1 potentially has a protective role in diabetic retinopathy.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.12-10921
Journal	Investigative Opthalmology & Visual Science
Issue Number	3
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-03-05
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Diabetic Retinopathy Genetics Micrornas Physiology Receptors, Neuropeptide Retina Metabolism Animals Apoptosis Cells, Cultured Diabetes Mellitus, Type 1 Disease Models, Animal Down-regulation Mice Mice, Inbred C57bl Oligonucleotide Array Sequence Analysis Orexin Receptors Oxidative Stress Rna, Messenger Real-time Polymerase Chain Reaction Transfection Tyrosine Analogs & Derivatives Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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