Static magnetic fields promote osteogenesis via the lncRNA Gas5/miR-182/PKR molecular axis in rat osteoblasts and femoral defect models

PURPOSE: Static magneticfields (SMF) stimulate osteogenesis, but the underlying mechanismremains unclear. This study investigated whether the lncRNAGas5/miR-182/PKR axis mediates SMF-enhanced osteogenic differentiation and bone repair. MATERIALS AND METHODS: Primary rat osteoblasts were induced with dexamethasone, ascorbic acid, and β-glycerolphosphate sodium, then exposed to 200 mT SMF or shamconditions. RT-PCR, Western blotting, ALP staining, alizarin redstaining, and dual-luciferase reporter assays were used to assessgene and protein expression, osteogenic markers, and lncRNAmiRNA binding. A femoral defect rat model was established, andtreated with SMF, lentiviral-mediated lncRNA Gas5 overexpression, or their combination. Bone formation was evaluated by Micro-CT, HE staining, and TRAP staining. Lentiviral vectors were used to over express lncRNA Gas5 in osteoblasts, and miR-182 mimicswere transfected to assess its role in osteogenesis. RESULTS: SMF increased BMP2 expression, ALP activity, and calcification nodulesin osteoblasts, indicating enhanced osteogenic differentiation. SMF upregulated lncRNA Gas5 and PKR, while down regulating miR-182. Dual-luciferase assays confirmed lncRNA Gas5 spongesmiR-182, which directly targets PKR mRNA. LncRNA Gas5 over expression promoted osteogenic markers (BMP-2, Runx2, OSX, OCN) and mineralization, with SMF enhancing this effect synergistically. In femoral defect models, combined SMF and lncRNA Gas5 treatment increased bone formation, as shown by Micro-CT and histological analysis. miR-182 over expression suppressed osteogenic proteins, which was rescued by lncRNAGas5 co-expression, confirming its role as a negative regulatorin the axis. CONCLUSIONS: SMF promotes osteogenesis and bone defect repair via the lncRNA Gas5/miR-182/PKR ceRNA pathway, revealing a novel epigenetic mechanism and a promising noninvasive therapy strategy.