Toxicon · 2021 · 13 citations · 15 references
T-2 ToxinApoptosisImmunologyImmune RegulationPathologyCell DeathOrthopaedic SurgeryMusculoskeletal ResearchInflammationSerum Bmp2 LevelsWnt/β-catenin Signalling PathwayBone Morphogenic ProteinCartilage DegenerationCell SignalingPaediatric Kashin-beck DiseaseInflammatory DiseaseCell BiologyCartilage InjuryMedicinePathway Induces
We investigated whether the WNT/β-catenin signalling pathway is involved in paediatric Kashin-Beck disease (KBD) and T-2-toxin-induced cartilage injury in rats to better understand the mechanism of KBD. One hundred twenty-two children were selected and assigned to the case (31), internal control (41), and external control (50) groups. The serum β-catenin and bone morphogenetic protein 2(BMP2)levels in each group were measured and compared. Thirty-six rats were randomly assigned to three groups, which received no intervention, T-2 toxin, or solvent. After 18 weeks, the expression of LDL receptor related proteins 5 (LRP5), β-catenin, BMP2, BAX, BCL2, APAF1, and caspase 9 was measured and compared. The serum BMP2 levels were significantly elevated in the children with KBD and in the rats treated with T-2 toxin. In the T-2 toxin group, LRP5 and β-catenin expression was reduced, whereas BAX, APAF1, and caspase 9 expression was increased. In conclusion, the WNT/β-catenin signalling pathway is suppressed in KBD, which induces chondrocyte apoptosis, leading to cartilage injury. Therefore, BMP2 may play a role in the pathogenesis of KBD.
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Binding of GSK3β to the APC-β-Catenin Complex and Regulation of Complex Assembly
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