Abstract
Hyperglycemia is generally considered to be an important cause of diabetic retinopathy (DR). The aim of the present study was to investigate the role of miR-5195-3p in high glucose (HG)-induced human retinal pigment epithelial ARPE-19 cell injury. Here, we first found that the expression level of miR-5195-3p was significantly downregulated in HG-stimulated ARPE-19 cells using reverse transcription quantitative PCR. Overexpression of miR-5195-3p attenuated the impaired cell viability, increased apoptosis and pro-inflammatory cytokines secretion in ARPE-19 cells under HG condition using CCK-8 assay, flow cytometry and ELISA assay, respectively. Luciferase reporter assay showed that miR-5195-3p could specifically bind to the 3’UTR of glia maturation factor-β (GMFB). GMFB overexpression reversed, while knockdown enhanced the protective effects of miR-5195-3p overexpression against HG-induced ARPE-19 cell injury. In summary, miR-5195-3p targeting GMFB might be a potential therapeutic target for DR.
Highlights
Diabetic retinopathy (DR) as a major complication of diabetes is one of the leading causes of vision loss and even blindness, which is characterized by retinal edema, neuronal dysfunction and breakdown of the blood–retinal barrier (BRB) [1,2]
We first determined the expression of miR-5195-3p and glia maturation factor-β (GMFB) in ARPE-19 cells under high glucose (HG) stimulation
Western blot results indicated that GMFB protein expression was obviously increased after HG treatment in ARPE-19 cells compared with control group (Fig 1B)
Summary
Diabetic retinopathy (DR) as a major complication of diabetes is one of the leading causes of vision loss and even blindness, which is characterized by retinal edema, neuronal dysfunction and breakdown of the blood–retinal barrier (BRB) [1,2]. Hyperglycemia as the main cause of the DR development can cause pathological metabolism and biochemical changes [3,4]. Retinal pigment epithelial (RPE) cells, an important cellular component of the outer BRB, could selectively control the flux of molecules into and out of the retina, which are most vulnerable to hyperglycemia [5,6,7]. Accumulating evidence has indicated the RPE dysfunction is relevant to the development of DR [8,9].
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