ArticleInternational journal of ophthalmology2026
MicroRNA-26a-5p inhibits high glucose-induced Müller cells apoptosis by mediating PTEN/PI3K/Akt pathway.
Article in International journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
aimTo investigate the functions of microRNA-26a-5p (miR-26a-5p) in the high glucose (HG)-induced rat retinal Müller cells (rMC-1) apoptosis and its possible mechanism.
methodsrMC-1 cells were transfected with miR-26a-5p mimics or phosphatase and tensin homolog (PTEN) siRNA under HG conditions. Cell apoptosis was analyzed by propidium iodide (PI) and annexin V fluorescein isothiocyanate (FITC) staining. PTEN/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway activation was assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot. Inflammatory cytokines, interleukin (IL)-1β, IL-6, were measured by enzyme-linked immunosorbent assay (ELISA). The miR-26a-5p-PTEN interaction was validated by dual-luciferase assay.
resultsHG significantly suppressed miR-26a-5p expression and induced apoptosis in rMC-1 cells. Overexpression of miR-26a-5p attenuated HG-induced apoptosis by directly targeting PTEN, as confirmed by dual-luciferase reporter assay, which demonstrated that miR-26a-5p directly binds to the PTEN 3'-UTR, resulting in a 50% reduction in luciferase activity (
conclusionUpregulation of miR-26a-5p protects rMC-1 from HG-induced apoptosis by targeting PTEN
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