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| 1 | Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect显示文摘Objective: To identify the relationship between T-2 toxin and Kashin-Beck disease (KBD),the effects of T-2 toxin on aggrecan metabolism in human chondrocytes and cartilage were investigated in vitro. Methods: Chondrocytes were isolated from human articular cartilage and cultured in vitro. Hyaluronic acid (HA),soluble CD44 (sCD44),IL-1β and TNF-α levels in super-natants were measured by enzyme-linked immunosorbent assay (ELISA). CD44 content in chondrocyte membrane was deter-mined by flow cytometry (FCM). CD44,hyaluronic acid synthetase-2 (HAS-2) and aggrecanases mRNA levels in chondrocytes were determined using reverse transcription polymerase chain reaction (RT-PCR). Immunocytochemical method was used to investigate expressions of BC-13,3-B-3(-) and 2-B-6 epitopes in the cartilage reconstructed in vitro. Results: T-2 toxin inhibited CD44,HAS-2,and aggrecan mRNA expressions,but promoted aggrecanase-2 mRNA expression. Meanwhile,CD44 expression was found to be the lowest in the chondrocytes cultured with T-2 toxin and the highest in control plus selenium group. In addition,ELISA results indicated that there were higher sCD44,IL-1β and TNF-α levels in T-2 toxin group. Similarly,higher HA levels were also observed in T-2 toxin group using radioimmunoprecipitation assay (RIPA). Furthermore,using monoclonal antibodies BC-13,3-B-3 and 2-B-6,strong positive immunostaining was found in the reconstructed cartilage cultured with T-2 toxin,whereas no positive staining or very weak staining was observed in the cartilage cultured without T-2 toxin. Selenium could partly inhibit the effects of T-2 toxin above. Conclusion: T-2 toxin could inhibit aggrecan synthesis,promote aggrecanases and pro-inflammatory cytokines production,and consequently induce aggrecan degradation in chondrocytes. These will perturb metabolism balance between aggrecan synthesis and degradation in cartilage,inducing aggrecan loss in the end,which may be the initiation of the cartilage degradation. | Si-yuan LI Jun-ling CAO Zhong-li SHI Jing-hong CHEN Zeng-tie ZHANG Clare E. HUGHES Bruce CATERSON | 2008 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2008，9，1： | 16 |
| 2 | Increased expression of chondroitin sulphate proteoglycans in rat hepatocellular carcinoma tissues显示文摘AIM:To investigate the expression of chondroitin sulphate proteoglycans(CSPGs)in rat liver tissues of hepatocellular carcinoma(HCC).METHODS:Thirty male Sprague Dawley rats were randomly divided into two groups:control group(n=10) and HCC model group(n=20).Rats in the HCC model groups were intragastrically administrated with 0.2%(w/v)N-diethylnitrosamine(DEN)every 5 d for 16 wk,whereas 0.9%(w/v)normal saline was administered to rats in the control group.After 16 wk from the initiation of experiment,all rats were killed and livers were collected and fixed in 4%(w/v)paraformaldehyde.All tissues were embedded in paraffin and sectioned.Histological staining(hematoxylin and eosin and Toluidine blue)was performed to demonstrate the onset of HCC and the content of sulphated glycosaminoglycan(sGAG).Immunohistochemical staining was performed to investigate the expression of chondroitin sulphate(CS)/dermatan sulphate(DS)-GAG,heparan sulphate(HS)-GAG,keratan sulphate(KS)-GAG in liver tissues.Furthermore,expression and distribution of CSPG family members,including aggrecan,versican,biglycan and decorin in liver tissues,were also immunohistochemically determined.RESULTS:After 16 wk administration of DEN,malignant nodules were observed on the surface of livers from the HCC model group,and their hepatic lobule structures appeared largely disrupted under microscope.Toluidine blue staining demonstrated that there was an significant increase in sGAG content in HCC tissues when compared with that in the normal liver tissues from the control group[0.37±0.05 integrated optical density per stained area(IOD/area)and 0.21± 0.01 IOD/area,P<0.05].Immunohistochemical studies demonstrated that this increased sGAG in HCC tissues was induced by an elevated expression of CS/DS(0.28±0.02 IOD/area and 0.18±0.02 IOD/area,P< 0.05)and HS(0.30±0.03 IOD/area and 0.17±0.02 IOD/area,P<0.01)but not KS GAGs in HCC tissues.Further studies thereby were performed to investigate the expression and distribution of several CSPG components in HCC tissues,including aggrecan,versican,biglycan and decorin.Interestingly,there was a distinct distribution pattern for these CSPG components between HCC tissues and the normal tissues.Positive staining of aggrecan,biglycan and decorin was localized in hepatic membrane and/or pericellular matrix in normal liver tissues;however,their expression was mainly observed in the cytoplasm,cell membranes in hepatoma cells and/or pericellular matrix within HCC tissues.Semi-quantitative analysis indicated that there was a higher level of expression of aggrecan(0.43± 0.01 and 0.35±0.03,P<0.05),biglycan(0.32±0.01 and 0.25±0.01,P<0.001)and decorin(0.29±0.01 and 0.26±0.01,P<0.05)in HCC tissues compared with that in the normal liver tissues.Very weak versican positive staining was observed in hepatocytes near central vein in normal liver tissues;however there was an intensive versican distribution in fibrosis septa between the hepatoma nodules.Semi-quantitative analysis indicated that the positive rate of versican in hepatoma tissues from the HCC model group was much higher than that in the control group(33.61%and 21.28%,P <0.05).There was no positive staining in lumican and keratocan,two major KSPGs,in either normal or HCC liver tissues.CONCLUSION:CSPGs play important roles in the onset and progression of HCC,and may provide potential therapeutic targets and clinical biomarkers for this prevalent tumor in humans. | Xiao-Li Jia Si-Yuan Li Shuang-Suo Dang Yan-An Cheng Xin Zhang Wen-Jun Wang Clare E Hughes Bruce Caterson | 2012 | World Journal of Gastroenterology2012，18，30： | 2 |
| 3 | Effects of culture conditions and exposure to catabolic stimulators (IL-1 and retinoic acid) on the expression of matrix metalloproteinases (MMPs) and disintegrin metalloproteinases (ADAMs) by articular cartilage chondrocytes显示文摘 | Carl R Flannery Chris B Little Bruce Caterson Clare E Hughes | 1999 | Matrix Biology1999，，3： | 1 |
| 4 | 大骨节病(发生在中国的一种地方性骨关节病)关节软骨代谢显示文摘目的本研究旨在了解大骨节病(KBD,在中国发生的一种地方性骨关节病)患者软骨CD44和蛋白聚糖的代谢及相关影响。方法用免疫组织化学方法分析分化抗原-44(CD44)、BC-13以及3-B-3(-)在所采集KBD患者和正常人软骨切片中的表达;采用夹心酶联免疫吸附测定法检测血清中可溶性CD44(sCD44)、白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)以及基质金属蛋白酶-1的水平。结果苏木素&伊红(HE)染色以及甲苯胺兰染色显示,在KBD病患儿以及成人软骨中有细胞坏死和蛋白聚糖的缺失;免疫组织化学染色发现,KBD成人和儿童患者软骨组织中CD44、BC-13和3-B-3(-)具很强的阳性表达;sCD44I、L-1β和TNF-α在KBD成人和儿童血清的水平明显高于正常成人及儿童对照组,经统计学分析具显著性差异。有意思的现象是,KBD病区正常儿童血清中IL-1β和TNF-α的水平亦明显高于非KBD病区正常儿童的水平,这些都提示可能还有一些未被确定的因素(例如遗传因素)或许对KBD发病具有一定的影响。结论大骨节病患者CD44I、L-1β和TNF-α代谢发生的改变,以及KBD成人和儿童软骨由于聚集蛋白聚糖酶活性增强所产生的蛋白聚糖的丢失,可能是KBD发病机理中起关键作用的重要因素,可以引起病态的关节形成和关节的不稳定,这些都可以导致在KBD患者中发生继发性的骨性关节炎。 | 曹峻岭 李思远 师钟丽 岳燕 孙健 陈静宏 付强 HUGHES Clare E CATERSON Bruce | 2009 | 西安交通大学学报(医学版)2009，30，2： | 1 |
| 5 | Comparison of synovial fluid cartilage marker concentrations and chondral damage assessed arthroscopically in acute knee injury显示文摘 | Alfonso E. Bello William E. Garrett Hao Wang John Lohnes Elizabeth DeLong Bruce Caterson Virginia B. Kraus | 1997 | Osteoarthritis and Cartilage1997，，6： | 1 |
| 6 | Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease显示文摘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. | An ZHANG Jun-ling CAO Bo YANG Jing-hong CHEN Zeng-tie ZHANG Si-yuan LI Qiang FU Clare E. HUGNES Bruce CATERSON | 2010 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2010，11，3： | 1 |
| 7 | Proteoglycan metabolism, cell death and Kashin-Beck Disease显示文摘 | Siyuan Li Junling Cao Bruce Caterson Clare E. Hughes | 2012 | Glycoconjugate Journal2012，，5： | 1 |
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