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Expression Profiles of Selenium-Related Genes in Human Chondrocytes Exposed to T-2 Toxin and Deoxynivalenol

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Abstract

The combination of excess mycotoxin exposure and selenium deficiency has been widely considered as a cause of Kashin-Beck disease (KBD). The present study aimed to investigate the expression profiles of selenium-related genes in human chondrocytes after exposure to T-2 toxin and deoxynivalenol (DON) and to preliminarily identify the potential biological functions of the identified genes. Gene expression profiling was performed on human chondrocytes treated with 0.01 μg/ml T-2 toxin and 1.0 μg/ml DON by using Affymetrix Human Gene Arrays. The 1660 selenium-related genes were derived from the Comparative Toxicogenomics Database. Gene-term enrichment analysis was conducted by the DAVID gene annotation tool. Our results showed that 69 and 191 selenium-related genes were differentially expressed after T-2 toxin and DON treatment, respectively. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that these identified genes were involved in various biological functions, such as the GO terms in response to oxidative stress, cell cycle arrest, and apoptotic process and the KEGG metabolic, FoxO signaling, and p53 signaling pathways. Our results may help explain the mechanisms of interaction between mycotoxins and selenium following human chondrocyte damage and reveal the potential roles of environmental risk factors in cartilage lesions during KBD development.

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References

  1. Tomlinson R (1999) Beijing conference reviews Kashin-Beck disease. BMJ 318(7182):485

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. National Health and Family Planning Commission (2015) China statistical yearbook of health and family planning. Pecking Union Medical College Press, Beijing

    Google Scholar 

  3. Guo X, Ma WJ, Zhang F, Ren FL, Qu CJ, Lammi MJ (2014) Recent advances in the research of an endemic osteochondropathy in China: Kashin-Beck disease. Osteoarthr Cartil 22(11):1774–1783. https://doi.org/10.1016/j.joca.2014.07.023

    Article  CAS  PubMed  Google Scholar 

  4. Guo X (2001) Diagnostic, clinical and radiological characteristics of Kashin-Beck disease in Shaanxi Province, PR China. Int Orthop 25(3):147–150

    Article  Google Scholar 

  5. Sudre P, Mathieu F (2001) Kashin-Beck disease: from etiology to prevention or from prevention to etiology? Int Orthop 25(3):175–179

    Article  CAS  PubMed  Google Scholar 

  6. Yang JB (1995) Research report on the etiology of Kashin-Beck disease. Chin J Endemiol 14:201–204

    Google Scholar 

  7. Lei R, Jiang N, Zhang Q, Hu S, Dennis BS, He S, Guo X (2015) Prevalence of selenium, T-2 toxin, and deoxynivalenol in Kashin-Beck disease areas in Qinghai province, northwest China. Biol Trace Elem Res 171(1):34–40. https://doi.org/10.1007/s12011-015-0495-0

    Article  CAS  PubMed  Google Scholar 

  8. Yang L, Zhao GH, Wang X, Wang YT, Lin XL, Yu FF, Goldring MB, Guo X, Lammi MJ (2017) Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes. Sci Rep 7(1):2231. https://doi.org/10.1038/s41598-017-02568-5

    Article  CAS  Google Scholar 

  9. Yang L, Zhao GH, Yu FF, Zhang RQ, Guo X (2016) Selenium and iodine levels in subjects with Kashin-Beck disease: a meta-analysis. Biol Trace Elem Res 170(1):43–54. https://doi.org/10.1007/s12011-015-0463-8

    Article  CAS  PubMed  Google Scholar 

  10. Lu M, Cao J, Liu F, Li S, Chen J, Fu Q, Zhang Z, Liu J, Luo M, Wang J, Li J, Caterson B (2012) The effects of mycotoxins and selenium deficiency on tissue-engineered cartilage. Cells Tissues Organs 196(3):241–250. https://doi.org/10.1159/000335046

    Article  CAS  PubMed  Google Scholar 

  11. Chen J, Chu Y, Cao J, Wang W, Liu J, Wang J (2011) Effects of T-2 toxin and selenium on chondrocyte expression of matrix metalloproteinases (MMP-1, MMP-13), alpha2-macroglobulin (alpha2M) and TIMPs. Toxicol in Vitro 25(2):492–499. https://doi.org/10.1016/j.tiv.2010.12.001

    Article  CAS  PubMed  Google Scholar 

  12. Yang L, Zhang J, Zhao G, Wu C, Ning Y, Wang X, Lammi MJ, Guo X (2017) Gene expression profiles and molecular mechanism of cultured human chondrocytes’ exposure to T-2 toxin and deoxynivalenol. Toxicon 140:38–44. https://doi.org/10.1016/j.toxicon.2017.06.014

    Article  CAS  PubMed  Google Scholar 

  13. Livak KJ, Schmittgen TD (2001) Analysis of relative gene expression data using real-time quantitative PCR and the 2(−Delta Delta C(T)) method. Methods 25:402–408. https://doi.org/10.1006/meth.2001.1262

    Article  CAS  PubMed  Google Scholar 

  14. Yang HJ, Zhang Y, Wang ZL, Xue SH, Li SY, Zhou XR, Zhang M, Fang Q, Wang WJ, Chen C, Deng XH, Chen JH (2017) Increased chondrocyte apoptosis in Kashin-Beck disease and rats induced by T-2 toxin and selenium deficiency. Biomed Environ Sci 30(5):351–362. https://doi.org/10.3967/bes2017.046

    Article  PubMed  Google Scholar 

  15. Cao JL, Xiong YM, Li SC (1993) The effect of seleniun and zinc on the growth of cultured chondrocytes. Chin J Endemiol 12(3):152–154

    Google Scholar 

  16. Duan C, Guo X, Zhang XD, Yu HJ, Yan H, Gao Y, Ma WJ, Gao ZQ, Xu P, Lammi M (2010) Comparative analysis of gene expression profiles between primary knee osteoarthritis and an osteoarthritis endemic to Northwestern China, Kashin-Beck disease. Arthritis Rheum 62(3):771–780. https://doi.org/10.1002/art.27282

    Article  PubMed  Google Scholar 

  17. Yan J, Zheng Y, Min Z, Ning Q, Lu S (2013) Selenium effect on selenoprotein transcriptome in chondrocytes. Biometals 26(2):285–296. https://doi.org/10.1007/s10534-013-9610-x

    Article  CAS  PubMed  Google Scholar 

  18. Wang X, Zuo Z, Deng J, Zhang Z, Chen C, Fan Y, Peng G, Cao S, Hu Y, Yu S, Chen C, Ren Z (2018) Protective role of selenium in immune-relevant cytokine and immunoglobulin production by piglet splenic lymphocytes exposed to deoxynivalenol. Biol Trace Elem Res 184(1):83–91. https://doi.org/10.1007/s12011-017-1160-6

    Article  CAS  PubMed  Google Scholar 

  19. Ahmadi A, Poursasan N, Amani J, Salimian J (2015) Adverse effect of T-2 toxin and the protective role of selenium and vitamin E on peripheral blood B lymphocytes. Iran J Immunol 12(1):64–69

    PubMed  Google Scholar 

  20. Shi D, Liao S, Guo S, Li H, Yang M, Tang Z (2015) Protective effects of selenium on aflatoxin B1-induced mitochondrial permeability transition, DNA damage, and histological alterations in duckling liver. Biol Trace Elem Res 163(1–2):162–168. https://doi.org/10.1007/s12011-014-0189-z

    Article  CAS  PubMed  Google Scholar 

  21. Fang J, Yin H, Zheng Z, Zhu P, Peng X, Zuo Z, Cui H, Zhou Y, Ouyang P, Geng Y, Deng J (2018) The molecular mechanisms of protective role of Se on the G2/M phase arrest of jejunum caused by AFB1. Biol Trace Elem Res 181(1):142–153. https://doi.org/10.1007/s12011-017-1030-2

    Article  CAS  PubMed  Google Scholar 

  22. Liu J, Wang L, Guo X, Pang Q, Wu S, Wu C, Xu P, Bai Y (2014) The role of mitochondria in T-2 toxin-induced human chondrocytes apoptosis. PLoS One 9(9):e108394. https://doi.org/10.1371/journal.pone.0108394

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Wu QH, Wang X, Yang W, Nussler AK, Xiong LY, Kuca K, Dohnal V, Zhang XJ, Yuan ZH (2014) Oxidative stress-mediated cytotoxicity and metabolism of T-2 toxin and deoxynivalenol in animals and humans: an update. Arch Toxicol 88(7):1309–1326. https://doi.org/10.1007/s00204-014-1280-0

    Article  CAS  PubMed  Google Scholar 

  24. Arunachalam C, Doohan FM (2013) Trichothecene toxicity in eukaryotes: cellular and molecular mechanisms in plants and animals. Toxicol Lett 217(2):149–158. https://doi.org/10.1016/j.toxlet.2012.12.003

    Article  CAS  PubMed  Google Scholar 

  25. Lorendeau D, Christen S, Rinaldi G, Fendt SM (2015) Metabolic control of signalling pathways and metabolic auto-regulation. Biol Cell 107(8):251–272. https://doi.org/10.1111/boc.201500015

    Article  CAS  PubMed  Google Scholar 

  26. Eelen G, Verlinden L, Maes C, Beullens I, Gysemans C, Paik JH, DePinho RA, Bouillon R, Carmeliet G, Verstuyf A (2016) Forkhead box O transcription factors in chondrocytes regulate endochondral bone formation. J Steroid Biochem Mol Biol 164:337–343. https://doi.org/10.1016/j.jsbmb.2015.07.015

    Article  CAS  PubMed  Google Scholar 

  27. Shen C, Cai GQ, Peng JP, Chen XD (2015) Autophagy protects chondrocytes from glucocorticoids-induced apoptosis via ROS/Akt/FOXO3 signaling. Osteoarthr Cartil 23(12):2279–2287. https://doi.org/10.1016/j.joca.2015.06.020

    Article  CAS  PubMed  Google Scholar 

  28. Wu C, Zheng J, Yao X, Shan H, Li Y, Xu P, Guo X (2014) Defective autophagy in chondrocytes with Kashin-Beck disease but higher than osteoarthritis. Osteoarthr Cartil 22(11):1936–1946. https://doi.org/10.1016/j.joca.2014.08.010

    Article  CAS  PubMed  Google Scholar 

  29. Yang G, Zhou X, Wang J, Zhang W, Zheng H, Lu W, Yuan J (2012) MEHP-induced oxidative DNA damage and apoptosis in HepG2 cells correlates with p53-mediated mitochondria-dependent signaling pathway. Food Chem Toxicol 50(7):2424–2431. https://doi.org/10.1016/j.fct.2012.04.023

    Article  CAS  PubMed  Google Scholar 

  30. Yu FF, Zhang YX, Zhang LH, Li WR, Guo X, Lammi MJ (2016) Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease. Medicine 95(52):e5669. https://doi.org/10.1097/md.0000000000005669

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Salvador JM, Brown-Clay JD, Fornace AJ Jr (2013) Gadd45 in stress signaling, cell cycle control, and apoptosis. Adv Exp Med Biol 793:1–19. https://doi.org/10.1007/978-1-4614-8289-5_1

    Article  CAS  Google Scholar 

Download references

Acknowledgements

This work was supported by the National Natural Scientific Foundation of China (nos. 81472924 and 81620108026) and the Fundamental Research Funds for the Central Universities (no. xjj2018154).

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Authors and Affiliations

  1. School of Nursing, Health Science Center, Xi’an Jiaotong University, Xi’an, 710061, Shaanxi, People’s Republic of China

    Lei Yang & Xiaomei Li

  2. School of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Xi’an Jiaotong University, Xi’an, 710061, Shaanxi, People’s Republic of China

    Lei Yang, Xi Wang & Xiong Guo

  3. Hainan Medical University, Haikou, 571199, Hainan, People’s Republic of China

    Jianping Zhang

  4. Traditional Chinese Medical Hospital of Linyou County, Baoji, 721500, Shaanxi, People’s Republic of China

    Chao Xu

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  1. Lei Yang
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  3. Xiaomei Li
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  4. Chao Xu
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  5. Xi Wang
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Correspondence to Xiong Guo.

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The authors declare that they have no conflict of interest.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards.

Electronic Supplementary Material

Table S1

The full list of differentially expressed selenium-related genes in human chondrocytes following T-2 toxin treatment (DOCX 15 kb)

Table S2

The full list of differentially expressed selenium-related genes in human chondrocytes following deoxynivalenol treatment (DOCX 19 kb)

Table S3

GO analysis of differentially expressed selenium-related genes in human chondrocytes upon exposure to T-2 toxin (XLSX 14 kb)

Table S4

GO analysis of differentially expressed selenium-related genes in human chondrocytes upon exposure to deoxynivalenol (XLSX 18 kb)

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Yang, L., Zhang, J., Li, X. et al. Expression Profiles of Selenium-Related Genes in Human Chondrocytes Exposed to T-2 Toxin and Deoxynivalenol. Biol Trace Elem Res 190, 295–302 (2019). https://doi.org/10.1007/s12011-018-1560-2

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  • DOI: https://doi.org/10.1007/s12011-018-1560-2

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