Landscape of microRNA in the aqueous humour of proliferative diabetic retinopathy as assessed by next‐generation sequencing. (30th May 2019)

• Record Type: Journal Article
• Authors: Chen, Shida; Yuan, Miner; Liu, Yaoming; Zhao, Xiujuan; Lian, Ping; Chen, Yang; Liu, Bingqian; Lu, Lin
• Is Part Of: Clinical & experimental ophthalmology. Volume 47:Number 7(2019)
• Page Start: 925
• Page End: 936
• Publication Date: 2019-05-30
• Subjects: biomarker -- microRNA -- next‐generation sequencing -- proliferative diabetic retinopathy -- piwi‐interacting RNA; Ophthalmology -- Periodicals; 617.7
• DOI: 10.1111/ceo.13554
• Languages: English
• ISSNs: 1442-6404

Abstract

Abstract: Background: The microRNAs (miRNA) have been found to play an important role in the pathogenesis of diabetic retinopathy. We try to explore the miRNA and piwi‐interacting RNA (piRNA) profile in the aqueous humour of proliferative diabetic retinopathy (PDR) using next‐generation sequencing (NGS). Methods: Aqueous humour samples were collected from nine PDR eyes and nine cataract control eyes, and NGS was performed. Quantitative polymerase chain reaction (qPCR) was used to validate the sequencing results. An oxygen‐induced retinopathy (OIR) model was used to validate the angiogenesis related miRNA. Results: In total, 484 miRNAs were differently expressed between the PDR eyes and cataract control eyes, including 210 mature miRNAs and 274 novel miRNAs. Furthermore, eight miRNAs and 30 piRNAs were identified as the most differently expressed between the two groups ( P > .85). This differential expression of miRNA was predicted to regulate Rho protein signal transduction, neurotransmitter uptake and histone lysine methylation. Relative expression patterns of miR‐184, ‐150‐5p and ‐93‐5p were confirmed by qPCR. A reduced expression of miR‐93‐5p was confirmed in the OIR model. Conclusions: This study comprehensively demonstrated the miRNA and piRNA expression profile of the aqueous humour of PDR eyes, which may serve as a potential biomarker and involved in the pathogenesis of PDR.