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MiR-214-3p may alleviate T-2 toxin-induced chondrocyte apoptosis and matrix degradation by regulating NF-κB signaling pathway in vitro.
- Source :
-
Toxicon . Mar2023, Vol. 225, pN.PAG-N.PAG. 1p. - Publication Year :
- 2023
-
Abstract
- T-2 toxin is part of the most toxic fungal secondary metabolites contaminating different kinds of grains. Previous studies have demonstrated that T-2 toxin can influence the survival of chondrocytes and extracellular matrix (ECM) composition. MiR-214-3p is essential for the homeostasis of chondrocytes and ECM. However, the molecular machinery underlying T-2 toxin-induced chondrocyte apoptosis and ECM degradation remain to be elucidated. The present study aimed to investigate the mechanism of miR-214-3p's involvement in T-2 toxin-induced chondrocyte apoptosis and ECM degradation. Meanwhile, the role of the NF-κB signaling pathway was scrutinized. C28/I2 chondrocytes were treated with 8 ng/ml of T-2 toxin for 24 h, after the pretreatment of miR-214-3p interfering RNAs for 6 h. Gene and protein levels involved in chondrocyte apoptosis and ECM degradation were assessed through RT-PCR and Western blotting. The apoptosis rate of chondrocyte was measured by flow cytometry. Results and data indicated that miR-214-3p was decreased in a dose-dependent manner at different concentrations of T-2 toxin. The enhancement of miR-214-3p could alleviate chondrocyte apoptosis and ECM degradation due to T-2 toxin exposure. The upregulation of miR-214-3p was associated with the decreased expression of apoptosis-promoting genes such as Bax and Cleaved-caspase3/caspase3 as well as the increased expression of anti-apoptotic genes such as Bcl2 and Survivin. Furthermore, miR-214-3p stimulated the relative protein expression of collagen Ⅱ but inhibited the expression of MMP13. Overexpressing miR-214-3p could suppress the relative protein expression of IKKβ and phospho-p65/p65, thus blocking the activation of the NF-κB signaling pathway. The study suggested that the miR-214-3p attenuates T-2 toxin-induced chondrocyte apoptosis and ECM degradation through a potential NF-κB signaling pathway. [Display omitted] • MiR-214-3p involved in T-2 toxin-induced chondrocyte apoptosis and ECM degradation. • Overexpressing miR-214-3p can alleviate T-2 toxin-induced chondrocyte apoptosis and ECM degradation. • Inhibiting miR-214-3p can aggravate T-2 toxin-induced chondrocyte apoptosis and ECM degradation. • Overexpressing miR-214-3p can inhibit the NF-κB signaling pathway. • Inhibiting miR-214-3p can activate the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00410101
- Volume :
- 225
- Database :
- Academic Search Index
- Journal :
- Toxicon
- Publication Type :
- Academic Journal
- Accession number :
- 162286698
- Full Text :
- https://doi.org/10.1016/j.toxicon.2023.107049