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Chondrocytes damage induced by T-2 toxin via Wnt/β-catenin signaling pathway is involved in the pathogenesis of an endemic osteochondropathy, Kashin-Beck disease.
Exp Cell Res. 2017 12 01; 361(1):141-148.EC

Abstract

Kashin-Beck disease (KBD), an endemic osteochondropathy, is characterized by cartilage degeneration which is caused by abnormal catabolism in the extracellular matrix (ECM). In this study, we investigated the expression of the Wnt/β-catenin signaling pathway in KBD pathogenesis. Among the proteins involved in the Wnt/β-catenin signaling pathway, WNT-3A, FZD1, SOX9, and β-catenin were up-regulated, while FRZB was down-regulated in KBD cartilage. C28/I2 cells were evaluated for cell viability using the MTT assay after exposure to T-2 toxin, a suspicious environmental pathogenic factors of KBD. C28/I2 cells were treated with different intervening concentrations (0.001μg/mL,0.005μg/mL and 0.01μg/mL) of T-2 toxin for 24h. The expression of FZD1 and CTNNB1 (i.e.,β-catenin) was significantly reduced and SOX9 expression was significantly increased in chondrocytes after treatment with different intervening concentrations of T-2 toxin. Our results indicate that alterations in the Wnt/β-catenin signaling pathway in articular cartilage play an important role in the onset and pathogenesis of KBD.

Authors+Show Affiliations

School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China; Xi'an Jiaotong University Global health institute, PR China.School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China.School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China.School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China.School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China.School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China. Electronic address: guox@xjtu.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29042209

Citation

Wang, Xi, et al. "Chondrocytes Damage Induced By T-2 Toxin Via Wnt/β-catenin Signaling Pathway Is Involved in the Pathogenesis of an Endemic Osteochondropathy, Kashin-Beck Disease." Experimental Cell Research, vol. 361, no. 1, 2017, pp. 141-148.
Wang X, Ning Y, Zhang P, et al. Chondrocytes damage induced by T-2 toxin via Wnt/β-catenin signaling pathway is involved in the pathogenesis of an endemic osteochondropathy, Kashin-Beck disease. Exp Cell Res. 2017;361(1):141-148.
Wang, X., Ning, Y., Zhang, P., Yang, L., Wang, Y., & Guo, X. (2017). Chondrocytes damage induced by T-2 toxin via Wnt/β-catenin signaling pathway is involved in the pathogenesis of an endemic osteochondropathy, Kashin-Beck disease. Experimental Cell Research, 361(1), 141-148. https://doi.org/10.1016/j.yexcr.2017.10.012
Wang X, et al. Chondrocytes Damage Induced By T-2 Toxin Via Wnt/β-catenin Signaling Pathway Is Involved in the Pathogenesis of an Endemic Osteochondropathy, Kashin-Beck Disease. Exp Cell Res. 2017 12 1;361(1):141-148. PubMed PMID: 29042209.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chondrocytes damage induced by T-2 toxin via Wnt/β-catenin signaling pathway is involved in the pathogenesis of an endemic osteochondropathy, Kashin-Beck disease. AU - Wang,Xi, AU - Ning,Yujie, AU - Zhang,Pan, AU - Yang,Lei, AU - Wang,Yingting, AU - Guo,Xiong, Y1 - 2017/10/16/ PY - 2017/08/16/received PY - 2017/10/12/revised PY - 2017/10/13/accepted PY - 2017/10/19/pubmed PY - 2017/12/13/medline PY - 2017/10/19/entrez KW - Chondrocytes KW - Kashin-Beck disease KW - T-2 toxin KW - Wnt/β-catenin signaling pathway SP - 141 EP - 148 JF - Experimental cell research JO - Exp. Cell Res. VL - 361 IS - 1 N2 - Kashin-Beck disease (KBD), an endemic osteochondropathy, is characterized by cartilage degeneration which is caused by abnormal catabolism in the extracellular matrix (ECM). In this study, we investigated the expression of the Wnt/β-catenin signaling pathway in KBD pathogenesis. Among the proteins involved in the Wnt/β-catenin signaling pathway, WNT-3A, FZD1, SOX9, and β-catenin were up-regulated, while FRZB was down-regulated in KBD cartilage. C28/I2 cells were evaluated for cell viability using the MTT assay after exposure to T-2 toxin, a suspicious environmental pathogenic factors of KBD. C28/I2 cells were treated with different intervening concentrations (0.001μg/mL,0.005μg/mL and 0.01μg/mL) of T-2 toxin for 24h. The expression of FZD1 and CTNNB1 (i.e.,β-catenin) was significantly reduced and SOX9 expression was significantly increased in chondrocytes after treatment with different intervening concentrations of T-2 toxin. Our results indicate that alterations in the Wnt/β-catenin signaling pathway in articular cartilage play an important role in the onset and pathogenesis of KBD. SN - 1090-2422 UR - https://www.unboundmedicine.com/medline/citation/29042209/Chondrocytes_damage_induced_by_T_2_toxin_via_Wnt/β_catenin_signaling_pathway_is_involved_in_the_pathogenesis_of_an_endemic_osteochondropathy_Kashin_Beck_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(17)30559-1 DB - PRIME DP - Unbound Medicine ER -