Effects of moniliformin and selenium on human articular cartilage metabolism and their potential rel

• 作 者: Clare E.HUGNES Bruce CATERSON
• 机 构: Laboratory of Connective Tissue Biology,School of Biosciences,Cardiff University Cardiff CF10 3US,UK
• 出 处: Journal of Zhejiang University-Science B(Biomedicine & Biote
• 发表日期: 2010年03期
• 关键词: cartilage articular metabolism selenium collagen inhibited pathogenesis gelatin

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.

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 o f aggrecan induced by MON toxin. Confluence: MON toxin promoted the catabolism of aggrecan and type II collagen in human chondrocytes.