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Inhibiting the aberrant activation of Wnt/β-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes.
J Cell Physiol. 2020 May; 235(5):4434-4442.JC

Abstract

Kashin-Beck disease (KBD) is an endemic degenerative osteoarticular disorder associated with physical disability and a heavy economic burden. Contamination by mycotoxin deoxynivalenol (DON) and selenium deficiency have been proposed to be key etiological factors for KBD, and can work together to aggravate the progression of KBD. Nevertheless, the mechanism of DON in KBD remains elusive. In the present study, exposure to DON dose-dependently suppressed cell viability and expression of pro-proliferation marker PCNA in human chondrocytes, whereas it enhanced lactate dehydrogenase release, cell apoptosis, and caspase-3/9 activity. In addition, DON incubation shifted metabolism homeostasis towards catabolism by suppressing the transcription of collagen II and aggrecan, and the production of sulphated glycosaminoglycans and TIMP-1, while increasing matrix metalloproteinase levels (MMP-1 and MMP-13). Mechanistically, DON exposure induced the activation of Wnt/β-catenin signaling. Intriguingly, blocking this pathway reversed the adverse effects of DON on cytotoxic damage and metabolism disruption to catabolism. Notably, supplementation with selenium reduced DON-induced activation of the Wnt/β-catenin pathway. Moreover, selenium addition abrogated cytotoxic injury and excessive pro-catabolic gene expression in chondrocytes upon DON conditions. These findings confirm that DON may facilitate the development of KBD by inducing cell injury, inhibiting matrix synthesis, and increasing cellular catabolism by activating the Wnt/β-catenin signaling, which were partially reversed by selenium supplementation. Thus, the current study may presents a new viewpoint for how selenium supplementation ameliorates the development of KBD by inhibiting DON-induced cytotoxic injury and metabolism imbalance in chondrocytes.

Authors+Show Affiliations

Outpatient Service Office, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.Department of Orthopaedics, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.Department of Orthopaedics, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.Department of Orthopaedics, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.Department of Integrative Medical Biology, University of Umeå, Umeå, Sweden.School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.Department of Orthopaedics, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31808557

Citation

Wang, Xiaoqing, et al. "Inhibiting the Aberrant Activation of Wnt/β-catenin Signaling By Selenium Supplementation Ameliorates Deoxynivalenol-induced Toxicity and Catabolism in Chondrocytes." Journal of Cellular Physiology, vol. 235, no. 5, 2020, pp. 4434-4442.
Wang X, Jin Z, Chen M, et al. Inhibiting the aberrant activation of Wnt/β-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes. J Cell Physiol. 2020;235(5):4434-4442.
Wang, X., Jin, Z., Chen, M., Duan, D., Lammi, M. J., Guo, X., & Chang, Y. (2020). Inhibiting the aberrant activation of Wnt/β-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes. Journal of Cellular Physiology, 235(5), 4434-4442. https://doi.org/10.1002/jcp.29319
Wang X, et al. Inhibiting the Aberrant Activation of Wnt/β-catenin Signaling By Selenium Supplementation Ameliorates Deoxynivalenol-induced Toxicity and Catabolism in Chondrocytes. J Cell Physiol. 2020;235(5):4434-4442. PubMed PMID: 31808557.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibiting the aberrant activation of Wnt/β-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes. AU - Wang,Xiaoqing, AU - Jin,Zhankui, AU - Chen,Ming, AU - Duan,Dapeng, AU - Lammi,Mikko J, AU - Guo,Xiong, AU - Chang,Yanhai, Y1 - 2019/12/06/ PY - 2019/05/28/received PY - 2019/09/30/accepted PY - 2019/12/7/pubmed PY - 2019/12/7/medline PY - 2019/12/7/entrez KW - Kashin-Beck disease KW - chondrocyte cytotoxic damage KW - deoxynivalenol KW - metabolism disorder KW - selenium SP - 4434 EP - 4442 JF - Journal of cellular physiology JO - J. Cell. Physiol. VL - 235 IS - 5 N2 - Kashin-Beck disease (KBD) is an endemic degenerative osteoarticular disorder associated with physical disability and a heavy economic burden. Contamination by mycotoxin deoxynivalenol (DON) and selenium deficiency have been proposed to be key etiological factors for KBD, and can work together to aggravate the progression of KBD. Nevertheless, the mechanism of DON in KBD remains elusive. In the present study, exposure to DON dose-dependently suppressed cell viability and expression of pro-proliferation marker PCNA in human chondrocytes, whereas it enhanced lactate dehydrogenase release, cell apoptosis, and caspase-3/9 activity. In addition, DON incubation shifted metabolism homeostasis towards catabolism by suppressing the transcription of collagen II and aggrecan, and the production of sulphated glycosaminoglycans and TIMP-1, while increasing matrix metalloproteinase levels (MMP-1 and MMP-13). Mechanistically, DON exposure induced the activation of Wnt/β-catenin signaling. Intriguingly, blocking this pathway reversed the adverse effects of DON on cytotoxic damage and metabolism disruption to catabolism. Notably, supplementation with selenium reduced DON-induced activation of the Wnt/β-catenin pathway. Moreover, selenium addition abrogated cytotoxic injury and excessive pro-catabolic gene expression in chondrocytes upon DON conditions. These findings confirm that DON may facilitate the development of KBD by inducing cell injury, inhibiting matrix synthesis, and increasing cellular catabolism by activating the Wnt/β-catenin signaling, which were partially reversed by selenium supplementation. Thus, the current study may presents a new viewpoint for how selenium supplementation ameliorates the development of KBD by inhibiting DON-induced cytotoxic injury and metabolism imbalance in chondrocytes. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/31808557/Inhibiting_the_aberrant_activation_of_Wnt/β_catenin_signaling_by_selenium_supplementation_ameliorates_deoxynivalenol_induced_toxicity_and_catabolism_in_chondrocytes_ L2 - https://doi.org/10.1002/jcp.29319 DB - PRIME DP - Unbound Medicine ER -
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