Mir-23A-3P Regulates Osteogenesis Via Lrp5 In Hpdlscs

This study investigates the regulatory role of miR-23a-3p in the osteogenic differentiation of human periodontal ligament stem cells (HPDLSCs) by targeting LRP5, using lentivirus-mediated inhibition/overexpression models. Understanding this pathway may provide insights into periodontal bone remodeling and therapeutic strategies. HPDLSCs were isolated from extracted premolars of orthodontic patients (12–20 years old) and characterized via morphological analysis, colony formation assays, and immunofluorescence staining. Lentiviral vectors were designed for miR-23a-3p overexpression/inhibition and LRP5 silencing. Transfection efficiency was determined by fluorescence microscopy and RT-qPCR. Osteogenic differentiation was induced, and the expression of LRP5, ALP, and RUNX2 was assessed by RT-qPCR and Western blot at multiple time points. Statistical significance was analyzed (p<0.05). 1. LRP5 expression peaked on day 7 of osteogenic induction and declined thereafter (p<0.01). 2. miR-23a-3p overexpression suppressed LRP5, ALP, and RUNX2 expression, while its inhibition promoted osteogenic differentiation (p<0.01). LRP5 silencing reduced osteogenic differentiation, confirming its role in the process. 3. The "miR-23a-3p inhibition + LRP5 silencing" model demonstrated that miR-23a-3p negatively regulates osteogenesis by targeting LRP5. This study successfully established lentiviral gene modulation models and demonstrated that miR-23a-3p inhibits osteogenic differentiation of HPDLSCs via LRP5 suppression. These findings provide a potential molecular target for periodontal bone regeneration strategies.