miR-103a-3p contributes to diabetic retinopathy progression via suppressing MFN2.
Diabetic retinopathy (DR), a complication of diabetes, damages microvascular of retina through various molecular pathways. Emerging evidence points to miRNAs as key players in progression of DR. This study aims to investigate whether miR-103a-3p contributes to pathological processes of DR through MFN2.
Serum samples were collected from type 2 diabetes mellitus patients and divided into NDR, NPDR, and PDR groups based on fundus lesions. miR-103a-3p levels in each group were quantified by qRT-PCR. ARPE-19 cells were cultured under high-glucose (HG). Cell viability and apoptosis rates were evaluated by CCK-8 assay and flow cytometry. Activities of MDA and GSH-Px were detected by specific kits. Luciferase reporter gene confirmed MFN2 as a direct target of miR-103a-3p.
Clinical sample detection revealed that miR-103a-3p levels were higher in NPDR and PDR patients compared to control and NDR groups, and it was an independent risk factor for DR. In vitro experiments confirmed that HG treatment greatly increased miR-103a-3p levels, decreased cell viability, accelerated apoptosis, elevated MDA content, and reduced GSH-Px activity, while transfection of miR-103a-3p inhibitor reversed these effects. Using luciferase reporter assay, we identified MFN2 as a direct target of miR-103a-3p. Moreover, rescue experiments demonstrated that silencing MFN2 effectively reversed the cell functions induced by miR-103a-3p inhibitor.
miR-103a-3p is upregulated in DR and accelerates its progression by directly targeting and inhibiting MFN2 expression. This study suggested the molecular mechanism of miR-103a-3p/MFN2 axis in DR, identifying a novel potential target for early diagnosis and therapy of DR.
Serum samples were collected from type 2 diabetes mellitus patients and divided into NDR, NPDR, and PDR groups based on fundus lesions. miR-103a-3p levels in each group were quantified by qRT-PCR. ARPE-19 cells were cultured under high-glucose (HG). Cell viability and apoptosis rates were evaluated by CCK-8 assay and flow cytometry. Activities of MDA and GSH-Px were detected by specific kits. Luciferase reporter gene confirmed MFN2 as a direct target of miR-103a-3p.
Clinical sample detection revealed that miR-103a-3p levels were higher in NPDR and PDR patients compared to control and NDR groups, and it was an independent risk factor for DR. In vitro experiments confirmed that HG treatment greatly increased miR-103a-3p levels, decreased cell viability, accelerated apoptosis, elevated MDA content, and reduced GSH-Px activity, while transfection of miR-103a-3p inhibitor reversed these effects. Using luciferase reporter assay, we identified MFN2 as a direct target of miR-103a-3p. Moreover, rescue experiments demonstrated that silencing MFN2 effectively reversed the cell functions induced by miR-103a-3p inhibitor.
miR-103a-3p is upregulated in DR and accelerates its progression by directly targeting and inhibiting MFN2 expression. This study suggested the molecular mechanism of miR-103a-3p/MFN2 axis in DR, identifying a novel potential target for early diagnosis and therapy of DR.