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Inhibiting the aberrant activation of Wnt/β-catenin signaling by selenium supplementation ameliorates deoxynivalenol-induced toxicity and catabolism in chondrocytes
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.
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2020 (Engelska)Ingår i: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 235, nr 5, s. 4434-4442Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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.

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell, 2020. Vol. 235, nr 5, s. 4434-4442
Nyckelord [en]
Kashin-Beck disease, chondrocyte cytotoxic damage, deoxynivalenol, metabolism disorder, selenium
Nationell ämneskategori
Cell- och molekylärbiologi Farmakologi och toxikologi Näringslära
Forskningsämne
cellforskning; mikrobiologi; näringslära
Identifikatorer
URN: urn:nbn:se:umu:diva-166033DOI: 10.1002/jcp.29319ISI: 000501028100001PubMedID: 31808557Scopus ID: 2-s2.0-85076100038OAI: oai:DiVA.org:umu-166033DiVA, id: diva2:1376183
Tillgänglig från: 2019-12-09 Skapad: 2019-12-09 Senast uppdaterad: 2020-03-30Bibliografiskt granskad

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Lammi, Mikko

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Institutionen för integrativ medicinsk biologi (IMB)
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Journal of Cellular Physiology
Cell- och molekylärbiologiFarmakologi och toxikologiNäringslära

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