Expression profiling of microRNAs in optineurin (E50K) mutant transgenic mice

Gao,Lin; Jiang,Bo; Lei,Dawei; Zhou,Xinrong; Yuan,Huiping

doi:10.3892/br.2015.565

Expression profiling of microRNAs in optineurin (E50K) mutant transgenic mice

Authors:
- Lin Gao
- Bo Jiang
- Dawei Lei
- Xinrong Zhou
- Huiping Yuan
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Affiliations: Department of Ophthalmology, The Second Affiliated Hospital, Harbin Medical University, Nangang, Harbin 150086, P.R. China
Published online on: December 31, 2015 https://doi.org/10.3892/br.2015.565
Pages: 193-196

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Abstract

An E50K substitution in the transcription factor optineurin (OPTN) induces primary open‑angle glaucoma (POAG). To explore the potential role of microRNAs (miRNAs) in E50K OPTN‑induced POAG, miRNA expression profiling was performed on retinal samples from OPTN (E50K) transgenic and wild‑type mice. The retinas were collected from 30 transgenic and 30 wild‑type mice, and miRNA expression was evaluated using a genome‑wide miRNA microarray. miRNAs that were differentially expressed in retinal samples from OPTN (E50K) transgenic mice were identified and validated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Additional gene ontology and signaling pathway analyses were performed using bioinformatics tools. A total of 48 miRNAs exhibited increased or decreased expression in the retinas from OPTN (E50K) transgenic mice when compared with the expression in the retinas from wild‑type mice. A total of 5 miRNAs with increased expression in OPTN (E50K) transgenic mice could be grouped into one cluster as they belong to the miR‑8 family and may act as regulators in the development of POAG in OPTN (E50K) transgenic mice. RT‑qPCR results confirmed significantly increased expression of miR‑141 in the retinas of OPTN (E50K) transgenic mice as compared to wild‑type mice. In conclusion, these results show that certain miRNAs are differentially expressed in the retinas of OPTN (E50K) transgenic mice and may play roles in the pathogenesis of POAG induced by OPTN (E50K).

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