CLC number: R684
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2010-02-03
Cited: 15
Clicked: 6192
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.
[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>