Full Text:   <1569>

CLC number: R684

On-line Access: 2010-03-10

Received: 2009-03-12

Revision Accepted: 2009-12-29

Crosschecked: 2010-02-03

Cited: 15

Clicked: 3279

Citations:  Bibtex RefMan EndNote GB/T7714

-   Go to

Article info.
1. Reference List
Open peer comments

Journal of Zhejiang University SCIENCE B 2010 Vol.11 No.3 P.200-208

10.1631/jzus.B0900074


Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease


Author(s):  An Zhang, Jun-ling Cao, Bo Yang, Jing-hong Chen, Zeng-tie Zhang, Si-yuan Li, Qiang Fu, Clare E. Hugnes, Bruce Caterson

Affiliation(s):  Institute of Endemic Diseases, School of Medicine, Xi’an Jiaotong University, Xi’an 710061, China, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Xi’an Jiaotong University, Xi’an 710061, China, Key Laboratory of Microelement and Endemic Disease of Ministry of Health, Xi’an Jiaotong University, Xi’an 710061, China, 4һLaboratory of Connective Tissue Biology, School of Biosciences, Cardiff University, Cardiff CF10 3US, UK

Corresponding email(s):   caojl@mail.xjtu.edu.cn, caterson@cardiff.ac.uk

Key Words:  Chondrocytes, Moniliformin, Selenium, Aggrecan, Collagen, Matrix metalloproteinases (MMPs), CD44, Kashin-Beck disease


An Zhang, Jun-ling Cao, Bo Yang, Jing-hong Chen, Zeng-tie Zhang, Si-yuan Li, Qiang Fu, Clare E. Hugnes, Bruce Caterson. Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease[J]. Journal of Zhejiang University Science B, 2010, 11(3): 200-208.

@article{title="Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease",
author="An Zhang, Jun-ling Cao, Bo Yang, Jing-hong Chen, Zeng-tie Zhang, Si-yuan Li, Qiang Fu, Clare E. Hugnes, Bruce Caterson",
journal="Journal of Zhejiang University Science B",
volume="11",
number="3",
pages="200-208",
year="2010",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B0900074"
}

%0 Journal Article
%T Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease
%A An Zhang
%A Jun-ling Cao
%A Bo Yang
%A Jing-hong Chen
%A Zeng-tie Zhang
%A Si-yuan Li
%A Qiang Fu
%A Clare E. Hugnes
%A Bruce Caterson
%J Journal of Zhejiang University SCIENCE B
%V 11
%N 3
%P 200-208
%@ 1673-1581
%D 2010
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B0900074

TY - JOUR
T1 - Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease
A1 - An Zhang
A1 - Jun-ling Cao
A1 - Bo Yang
A1 - Jing-hong Chen
A1 - Zeng-tie Zhang
A1 - Si-yuan Li
A1 - Qiang Fu
A1 - Clare E. Hugnes
A1 - Bruce Caterson
J0 - Journal of Zhejiang University Science B
VL - 11
IS - 3
SP - 200
EP - 208
%@ 1673-1581
Y1 - 2010
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B0900074


Abstract: 
Objective: To investigate the effects of mycotoxin moniliformin (MON) on the metabolism of aggrecan and type II collagen in human chondrocytes in vitro and the relationship between MON and kashin-Beck disease (KBD). Methods: Human chondrocytes were isolated and cultured on bone matrix gelatin to form an artificial cartilage model in vitro with or without MON toxin. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of aggrecan and type II collagen in the cartilage was determined using immunocytochemical staining. Results: MON toxin inhibited chondrocyte viability in dose-dependent and time-dependent manners. MON reduced aggrecan and type II collagen syntheses in the tissue-engineered cartilage. MON also increased the expression of matrix metalloproteinase-1 (MMP-1), MMP-13, BC4 epitopes, and CD44 in cartilages. However, the expression of 3B3(−) epitopes in cartilages was inhibited by MON. selenium partially alleviated the damage of aggrecan induced by MON toxin. Conclusion: MON toxin promoted the catabolism of aggrecan and type II collagen in human chondrocytes.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Aigner, T., Stöve, J., 2003. Collagens—major component of the physiological cartilage matrix, major target of cartilage degeneration, major tool in cartilage repair. Adv. Drug Del. Rev., 55(12):1569-1593.

[2]Cao, J.L., Mo, X.Y., Wang, C.Y., 1994. Effects of selenium and zinc on the growth metabolism of cultured chondrocytes. Chin. J. Endemiol., 14(10):628-630 (in Chinese).

[3]Cao, J.L., Zheng, B., Zhang, S.Y., Mo, D.X., 1995. The experimental study of moniliformin effects on the chondrocytes. Endemic. Dis. Bull., 10(4):5-7 (in Chinese).

[4]Cao, J.L., Zhang, A., Yang, B., Zhang, Z.T., Fu, Q., Hughes, C.E., Caterson, B., 2007. The effect of fungal moniliformin toxin and selenium supplementation on cartilage metabolism in vitro. Osteoarthritis and Cartilage, 15(Suppl. 3):C108.

[5]Cao, J.L., Li, S., Shi, Z., Yue, Y., Sun, J., Chen, J., Fu, Q., Hughes, C.E., Caterson, B., 2008. Articular cartilage metabolism in patients with Kashin-Beck disease: an endemic osteoarthropathy in China. Osteoarthritis and Cartilage, 16(6):680-688.

[6]Caterson, B., Mahmoodian, F., Sorrel, J.M., Hardingham, T.E., Bayliss, M.T., Carney, S.L., Ratcliffe, A., Muir, H., 1990. Modulation of native chondroitin sulfate structure in tissue development and in disease. Cell Sci., 97(3):411-417.

[7]Caterson, B., Carl, R.F., Clare, E.H., Chris, B.L., 2000. Mechanisms involved in cartilage proteoglycan catabolism. Matr. Biol., 19(4):333-344.

[8]Cetin, Y., Bullerman, L.B., 2005. Cytotoxicity of fusarium mycotoxins to mammalian cell cultures as determined by the MTT bioassay. Food Chem. Toxicol., 43(5):755-764.

[9]Chan, P., Wu, C., 2006. A peptide fragment of type II collagen induces the OA phenotype. Matr. Biol., 25(Supp. 1):S44.

[10]Chen, J.H., Chu, Y.L., Cao, J.L., Yang, Z.T., Guo, X., Wang, Z.L., 2006. T-2 toxin induces apoptosis, and selenium partly blocks, T-2 toxin induced apoptosis in chondrocytes through modulation of the Bax/Bcl-2 ratio. Food Chem. Toxicol., 44(4):567-573.

[11]Gelse, K., Poschl, E., Aigner, T., 2003. Collagens—structure, function, and biosynthesis. Adv. Drug Del. Rev., 55(12): 1531-1546.

[12]Hayes, A.J., Hughes, C.E., Caterson, B., 2008. Antibodies and immunohistochemistry in extracellular matrix research. Methods, 45(1):10-21.

[13]Khan, I.M., Gilbert, S.J., Caterson, B., Sandell, L.J., Archer, C.W., 2008. Oxidative stress induces expression of osteoarthritis markers procollagen IIA and 3B3(−) in adult bovine articular cartilage. Osteoarthritis and Cartilage, 16(6):698-707.

[14]Knudson, C.B., Knudson, W., 2001. Cartilage proteoglycans. Sem. Cell Dev. Biol., 12(2):69-78.

[15]Li, S.J., Yang, L.S., Li, Y.H., Wang, W.L., Xirao, R.D., 2006. Relationship between the content of selenium in grains and the Kaschin-Beck disease in Tibet China. Chin. J. Endemiol., 25(6):673-674 (in Chinese).

[16]Li, S.Y., Cao, J.L., Shi, Z.L., Chen, J.H., Zhang, Z.T., Hughes, C.E., Caterson, B., 2008. Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect. J. Zhejiang Univ.-Sci. B, 9(1): 22-33.

[17]Li, X.D., Li, J., Balian, G., Laurencin, C.T., Anderson, D.G., 2006. Demineralized bone matrix gelatinas scaffold for osteochondral tissue engineering. Biomaterials, 27(11): 2426-2433.

[18]Lin, P.M., Chen, C.T.C., Torzilli, P.A., 2004. Increased stromelysin-1 (MMP-3), proteoglycan degradation (3B3- and 7D4) and collagen damage in cyclically load-injured articular cartilage. Osteoarthritis and Cartilage, 12(6):485-496.

[19]Little, C.B., Hughes, C.E., Curtis, C.L., Janusz, M.J., Bohne, R., Wang-Weigand, S., Taiwo, Y.O., Mitchell, P.G., Otterness, I.G., Flannery, G.R., Caterson, B., 2002. Matrix metalloproteinases are involved in C-terminal and interglobular domain processing of cartilage aggrecan in late stage cartilage degradation. Matr. Biol., 21(3):271-288.

[20]Mario Geysen, H., 1985. Antigen-antibody interactions at the molecular level: adventures in peptide synthesis. J. Immunol. Today, 6(12):364-369.

[21]Mo, D.X., Ding, D.X., Wang, Z.L., Zhang, J., Bai, C., 1997. Twenty-year research on selenium related to Kashin-Beck Disease. Xi’an Med. Univ., 9(1):79-89 (in Chinese).

[22]Moreno, R.R., 2009. Iodine, Selenium Deficiency and Kashin-Beck Disease. Comprehensive Handbook of Iodine. Nutritional, Biochemical, Pathological and Therapeutic Aspects, Brussels, Belgium, p.685-700.

[23]Nathanson, M.A., Robert Hilfer, S., Searls, R.L., 1978. Formation of cartilage by non-chondrogenic cell types. Dev. Biol., 64(1):99-117.

[24]National KBD Surveillance Group, 2001. The monitoring report of KBD prevalence rate of the whole country in 2001. Chin. J. Endemiol., 20(5):350-353 (in Chinese).

[25]Ra, H.J., Parks, W.C., 2007. Control of matrix metalloproteinase catalytic activity. Matr. Biol., 26(8):587-596.

[26]Roughley, P., Hoemann, C., Rosiers, E.D., Mwale, F., Antoniou, J., Alini, M., 2006. The potential of chitosan-based gels containing intervertebral disc cells for nucleus pulposus supplementation. Biomaterials, 27(3):388-396.

[27]Shi, Z.L., Cao, J.L., Chen, J.H., Li, S.Y., Zhang, Z.T., Yang, B., Peng, S.Q., 2009. Butenolide induced cytotoxicity by disturbing the prooxidant-antioxidant balance, and antioxidants partly quenchin human chondrocytes. Toxicol. in Vitro, 23(1):99-104.

[28]Slater, R.R., Michael, T., Bayliss, M.T., Lachiewicz, P.F., Visco, D.M., Caterson, B., 1995. Monoclonal antibodies that detect biochemical markers of arthritis in humans. Arthritis Rheum., 38(5):655-659.

[29]Stadtman, L.C., 1980. Biological functions of selenium. Trends Biochem. Sci., 5(8):203-206.

[30]Stanton, H., Fosang, A.J., 2002. Matrix metalloproteinases are active following guanidine hydrochloride extraction of cartilage: generation of DIPEN neoepitope during dialysis. Int. Soc. Matr. Biol., 21(5):425-428.

[31]Sumer, E.U., Sondergaard, B.C., Rousseau, J.C., Delmas, P.D., Fosang, A.J., Karsdal, M.A., Christiansen, C., Qvist, P., 2007. MMP and non-MMP-mediated release of aggrecan and its fragments from articular cartilage: a comparative study of three different aggrecan and glycosaminoglycan assays. Osteoarthritis and Cartilage, 15(5):594-595.

[32]Tadashi, Y., Elena, T., Kunitaka, O., Peter, J.R., William, W., Aisha, M., Mirela, I., Isabelle, P., Robin, P.A., 2006. Peptides of type II collagen can induce the cleavage of type II collagen and aggrecan in articular cartilage. Int. Soc. Matr. Biol., 25:419-429.

[33]Tan, J.A., Zhu, W.Y., Wang, W.Y., Li, R.B., Hou, S.F., Wang, D.H., Yang, L.S., 2002. Selenium in soil and endemic diseases in China. Sci. Total Environ., 284(1-3):227-235.

[34]Warren, K., Geraldine, C., Cheryl, B.K., 2002. CD44-mediated uptake and degradation of hyaluronan. Int. Soc. Matr. Biol., 21:15-23.

[35]Xiong, Y.M., Mo, D.X., Li, S.C., Guo, X., Zhang, S.Y., Wang, Z.L., Bi, H.Y., Xu, J.R., 1998. The experimental study of moniliformin and selenium effects on articular cartilage of Chinese experimental mini pig. Endemic Dis. Bull., 3(2):1-3 (in Chinese).

[36]Yang, J.B., 2002. Mycotoxins and human diseases. Chin. J. Endemiol., l21(4):314-317 (in Chinese).

[37]Zhao, X.J., 2002. Research progress moniliformin. Progress in Veterinary Medicine, 23(4):19-22.

Open peer comments: Debate/Discuss/Question/Opinion

<1>

Please provide your name, email address and a comment





Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou 310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn
Copyright © 2000 - Journal of Zhejiang University-SCIENCE