Low-frequency electromagnetic fields ameliorate testosterone-induced androgenetic alopecia in mice through LncRNA H19/miR-214-5p/β-catenin signal pathway

Background In androgenetic alopecia (AGA), the depletion or long-term inactivity of the hair follicle stem cells (HFSCs) pool is a fundamental cause. Reviving inactive HFSCs is regarded as a promising treatment method for hair loss. Objective This study explored whether applying low-frequency electromagnetic fields (LFEMF) (1 Hz and 50 Hz) externally can enhance the activation and proliferation of HFSCs and alleviate symptoms of AGA in mice via the LncRNA H19/miR-214-5p/β-catenin signal pathway. Methods Scalp samples were obtained from 30 AGA patients and 30 healthy controls. The levels of LncRNA H19, miR-214-5p and β-catenin were assessed using qRT-PCR and Western blotting. Male C57BL/6 mice were employed to generate a dihydrotestosterone (DHT)-induced AGA model, while HFSCs were served to construct a DHT-induced in vitro cellular model. Subsequently, the effects and underlying mechanisms of LFEMFs treatment were examined through immunohistochemistry, direct observation of hair growth, cell proliferation assays, cell cycle and apoptosis analysis, as well as qRT-PCR and Western blotting. The relationship between LncRNA H19, miR-214-5p and β-catenin were further explored using RNA pull-down, RNA-binding protein immunoprecipitation (RIP), fluorescence in situ hybridization (FISH), and luciferase reporter assay. Results LFEMF stimulated hair regeneration in mice and reversed DHT-induced cell apoptosis by activating LncRNA H19/miR-214-5p/β-catenin signaling pathway. Conclusion LFEMF alleviates DHT-induced AGA and stimulates hair regrowth in mice by activating Wnt/β-catenin signaling pathway, suggesting its potential as a therapeutic strategy for AGA.