Litcius/Paper detail

The WNT/β-catenin signalling pathway induces chondrocyte apoptosis in the cartilage injury caused by T-2 toxin in rats

Tongkun Shi, Xiaoyan Fu, Fenghua Wang, Xin Zhang, Yun Cai, Xianhao Wu, Liyan Sun

2021Toxicon14 citationsDOIOpen Access PDF

Abstract

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.

Topics & Concepts

ChondrocyteCateninWnt signaling pathwayApoptosisCartilageToxinBone morphogenetic protein 2LRP5Internal medicineMedicineEndocrinologyChemistryCancer researchSignal transductionBiologyImmunologyCell biologyAnatomyMicrobiologyBiochemistryIn vitroSelenium in Biological SystemsPhytase and its Applications
The WNT/β-catenin signalling pathway induces chondrocyte apoptosis in the cartilage injury caused by T-2 toxin in rats | Litcius