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miR-103a-3p contributes to diabetic retinopathy progression via suppressing MFN2
Yidan Liu1, Yan Zhao2, Jinling Liu3
1Geriatric Center, Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, 010050, China.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
Insights
MicroRNA-103a-3p (miR-103a-3p) is elevated in diabetic retinopathy (DR) and worsens the condition by targeting MFN2. This miR-103a-3p/MFN2 pathway offers a new target for DR diagnosis and treatment.
Area of Science:
- Ophthalmology
- Molecular Biology
- Endocrinology
Background:
- Diabetic retinopathy (DR) is a diabetes complication damaging retinal microvasculature.
- MicroRNAs (miRNAs) are implicated in DR progression.
- This study investigates miR-103a-3p's role in DR via MFN2.
Purpose of the Study:
- To explore the contribution of miR-103a-3p to diabetic retinopathy pathogenesis.
- To elucidate the molecular mechanism involving miR-103a-3p and MFN2 in DR.
- To identify potential diagnostic and therapeutic targets for DR.
Main Methods:
- Serum samples from type 2 diabetes mellitus patients (NDR, NPDR, PDR) were analyzed for miR-103a-3p levels using qRT-PCR.
- ARPE-19 cells were cultured under high-glucose conditions to assess cell viability, apoptosis, MDA, and GSH-Px activity.
- Luciferase reporter assays and rescue experiments were performed to confirm MFN2 as a direct target of miR-103a-3p.
Main Results:
- miR-103a-3p levels were significantly higher in NPDR and PDR patients and identified as an independent risk factor for DR.
- High-glucose exposure increased miR-103a-3p, reduced cell viability, increased apoptosis, and altered MDA/GSH-Px levels; miR-103a-3p inhibition reversed these effects.
- MFN2 was confirmed as a direct target, and its silencing reversed miR-103a-3p inhibitor-induced cellular changes.
Conclusions:
- miR-103a-3p is upregulated in DR and promotes its progression by inhibiting MFN2 expression.
- The miR-103a-3p/MFN2 axis plays a crucial role in the molecular mechanisms of DR.
- This axis represents a novel potential target for the early diagnosis and therapy of DR.
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