ArticleMammalian genome : official journal of the International Mammalian Genome Society2026
Regulation of humeral fracture healing by miR-21 through SMAD7-mediated activation of Wnt/β-catenin signaling.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
MicroRNAs (miRNAs) are key regulators of bone regeneration. We investigated the role of miR-21 in humeral fracture (HF) healing, focusing on its interaction with the SMAD7/Wnt/β-catenin signaling axis. Serum and tissue levels of miR-21 were analyzed in HF patients and healthy controls using qRT-PCR. A rat HF model was established, and agomiR-21 was administered to evaluate its effect on fracture healing. Histological analysis using hematoxylin and eosin (H&E) staining was performed to assess bone tissue morphology and fracture healing. In vitro, MC3T3-E1 osteoblasts were transfected with miR-21 mimics to assess cell viability (CCK-8), proliferation (EdU), apoptosis (flow cytometry), migration (Transwell assay), and osteogenic differentiation (Western blot). The downstream target of miR-21 was identified using bioinformatics and validated via luciferase reporter and RNA immunoprecipitation assays. Rescue experiments involving SMAD7 overexpression and Wnt/β-catenin inhibitors (DKK1) were conducted to explore the mechanism of action. Serum analysis revealed reduced β-catenin and phosphorylated GSK3β (p-GSK3β) levels in humeral fracture (HF) patients compared to healthy controls, indicating suppressed Wnt/β-catenin signaling. In MC3T3-E1 cells, miR-21 overexpression enhanced osteogenic markers and increased total β-catenin, active β-catenin, and p-GSK3β levels, confirming activation of the Wnt/β-catenin pathway. Dual-luciferase and expression analyses demonstrated that miR-21 directly targets SMAD7, a known Wnt pathway inhibitor. Co-transfection with SMAD7 reversed the effects of miR-21 on β-catenin activation, ALP activity, and osteogenic gene expression. Additionally, miR-21 knockdown impaired osteogenesis, further supporting its regulatory role. Importantly, in vivo, agomiR-21 treatment enhanced osteoblast activity and significantly promoted bone healing in a rat fracture model, reinforcing the therapeutic potential of miR-21-mediated SMAD7 suppression and Wnt/β-catenin pathway activation in bone regeneration. miR-21 promotes bone regeneration after humeral fracture by enhancing osteoblast function and activating Wnt/β-catenin signaling through direct inhibition of SMAD7.
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