miR-10b-5p alleviates type 2 diabetic retinopathy by targeting PTBP1

Although diabetic retinopathy (DR) is a prevalent microvascular complication of type 2 diabetes (T2DM), the specific role of miR-10b-5p in this process is not well defined. This study was designed to investigate the diagnostic potential of serum miR-10b-5p for DR and to elucidate its underlying molecular mechanisms related to PTBP1. This study recruited 270 patients with type 2 diabetes, comprising 90 patients with non-DR (NDR), 93 patients with non-proliferative DR (NPDR), and 87 patients with proliferative DR (PDR). qRT-PCR was used to detect the expression of miR-10b-5p/PTBP1. A high glucose (HG)-induced injury model of human retinal microvascular endothelial cells (HRMECs) was constructed. Cell proliferation, migration, and apoptosis were evaluated after transfection with miR-10b-5p mimics or PTBP1 overexpression plasmids. The targeting relationship between miR-10b-5p and PTBP1 was analyzed by dual-luciferase reporter assay. The expression level of miR-10b-5p in DR patients was significantly lower than that in NDR, with an AUC of 0.856. Its expression was lowest in the PDR group and negatively correlated with serum VEGF and endothelial cell count. Low miR-10b-5p was an independent risk factor for PDR (OR = 0.109). In HRMECs, HG suppressed miR-10b-5p expression. Overexpression of miR-10b-5p partially reversed the high-glucose-induced declines in cell viability and migratory capacity, as well as the elevation of apoptotic rate in HRMECs. Mechanistically, miR-10b-5p directly targeted and inhibited PTBP1. Overexpression of PTBP1 reversed the protective effects of miR-10b-5p. Downregulated serum miR-10b-5p is associated with DR and PDR, suggesting its potential utility as a diagnostic biomarker. By targeting PTBP1, miR-10b-5p protects against HG-induced endothelial dysfunction in vitro, warranting further in vivo investigation of this axis. Not applicable.