@article{Shi2026, 
author = {Rui Shi and De-Rong Tang and Di Li and Yu-Wen Yang and Hong-Bo Li and Dan-Dan Liu and Xiao-Yu Gong and Jing Qin},
title = {MicroRNA-26a-5p inhibits high glucose-induced Müller cells apoptosis by mediating PTEN/PI3K/Akt pathway},
year = {2026},
journal = {International Journal of Ophthalmology},
volume = {19},
number = {10},
pages = {1929-1938},
keywords = {microRNA-26a-5p, phosphatase and tensin homolog, Müller cell, PI3K/Akt pathway, apoptosis, high glucose},
url = {https://www.sciopen.com/article/10.18240/ijo.2026.10.06},
doi = {10.18240/ijo.2026.10.06},
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 (P<0.01). Consistent with this, miR-26a-5p overexpression downregulated PTEN expression, enhanced PI3K/Akt phosphorylation, and suppressed the secretion of IL-1β and IL-6 (all P<0.01).CONCLUSIONUpregulation of miR-26a-5p protects rMC-1 from HG-induced apoptosis by targeting PTEN via regulating the PI3K/Akt pathway and inflammatory responses. miR-26a-5p may be a potential therapeutic target for diabetic retinal neurodegeneration.}
}