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Cytotoxic properties of HT-2 toxin in human chondrocytes: Could T3 inhibit toxicity of HT-2?
School of Public Health, Health Science Center of Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health Commission of the People's Republic of China, Xi'an, China.
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). School of Public Health, Health Science Center of Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health Commission of the People's Republic of China, Xi'an, China. (Chondrogenic and Osteogenic Differentiation)ORCID iD: 0000-0002-6181-9904
School of Public Health, Health Science Center of Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health Commission of the People's Republic of China, Xi'an, China.
School of Public Health, Health Science Center of Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health Commission of the People's Republic of China, Xi'an, China.
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2019 (English)In: Toxins, ISSN 2072-6651, E-ISSN 2072-6651, Vol. 11, no 11, p. E667-E667, article id 31731600Article in journal (Refereed) Published
Abstract [en]

Thyroid hormone triiodothyronine (T3) plays an important role in coordinated endochondral ossification and hypertrophic differentiation of the growth plate, while aberrant thyroid hormone function appears to be related to skeletal malformations, osteoarthritis, and Kashin-Beck disease. The T-2 toxin, present extensively in cereal grains, and one of its main metabolites, HT-2 toxin, are hypothesized to be potential factors associated with hypertrophic chondrocyte-related osteochondropathy, known as the Kashin-Beck disease. In this study, we investigated the effects of T3 and HT-2 toxin on human chondrocytes. The immortalized human chondrocyte cell line, C-28/I2, was cultured in four different groups: controls, and cultures with T3, T3 plus HT-2 and HT-2 alone. Cytotoxicity was assessed using an MTT assay after 24-h-exposure. Quantitative RT-PCR was used to detect gene expression levels of collagen types II and X, aggrecan and runx2, and the differences in runx2 were confirmed with immunoblot analysis. T3 was only slightly cytotoxic, in contrast to the significant, dose-dependent cytotoxicity of HT-2 alone at concentrations ≥ 50 nM. T3, together with HT-2, significantly rescued the cytotoxic effect of HT-2. HT-2 induced significant increases in aggrecan and runx2 gene expression, while the hypertrophic differentiation marker, type X collagen, remained unchanged. Thus, T3 protected against HT-2 induced cytotoxicity, and HT-2 was an inducer of the pre-hypertrophic state of the chondrocytes.

Place, publisher, year, edition, pages
MDPI, 2019. Vol. 11, no 11, p. E667-E667, article id 31731600
Keywords [en]
HT-2 toxin, Kashin-Beck disease, cytotoxicity, triiodothyronine
National Category
Pharmacology and Toxicology Rheumatology and Autoimmunity Cell and Molecular Biology
Research subject
cell research; Toxicology; rheumatology
Identifiers
URN: urn:nbn:se:umu:diva-165246DOI: 10.3390/toxins11110667PubMedID: 31731600OAI: oai:DiVA.org:umu-165246DiVA, id: diva2:1370706
Available from: 2019-11-17 Created: 2019-11-17 Last updated: 2019-11-26Bibliographically approved

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Lammi, Mikko

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