title: Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis.
abstract: OBJECTIVE
  Kashin-Beck disease (KBD) is an endemic degenerative osteoarthritis associated with extracellular matrix degradation. The aim of this investigation was to evaluate the role of targeting genes in the pathogenesis of KBD and primary osteoarthritis (OA) involved in extracellular matrix degradation.
  
  
  METHODS
  Agilent 44 K human whole-genome oligonucleotide microarrays were used to detect the gene expression in KBD and OA cartilage. The mRNA and protein expressions of CSGalNAcT-1 and Hapln-1 in chondrocytes were verified by reverse transcription polymerase chain reaction (RT-PCR) and western blot, and their expression in cartilage were verified with immunocytochemical analysis. Meanwhile, CSGalNAcT-1 and Hapln-1 protein levels in the selenium intervention group of KBD with different concentrations (0.25, 0.1 and 0.05 μg/ml) were detected by western blot.
  
  
  RESULTS
  CSGalNAcT-1 and Hapln-1 were down-regulated in KBD and OA at both mRNA and protein levels, and were increased in Se(Selenium) groups compared to KBD free-Se group. However, Wnt 3a, β-catenin and Runx-2 were up-regulated in OA and KBD at protein levels. Additionally, immunohistochemical staining showed that CSGalNAcT-1 and Hapln-1 were reduced in all zones of KBD and OA articular cartilage, but not significantly reduced in the up zone of OA articular cartilage.
  
  
  CONCLUSIONS
  The CSGalNAcT-1 and Hapln-1 were down-regulated in both KBD and OA cartilage. CSGalNAcT-1 may be involved in the damage of articular cartilage of KBD and OA by regulating Hapln-1 in the Wnt/β-catenin signalling pathway. It was indicated that CSGalNAcT-1 and Hapln-1 may play important roles in the pathogenesis of KBD and OA.
authors.affiliation: Faculty of Public Health, Medicine College of Xi'an Jiaotong University; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education; Key Laboratory of Trace elements and Endemic Diseases, Ministry of Health, Xi'an, Shaanxi, 710061, People's Republic of China.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Zheng
authors.forename: Cuiyan
authors.initials: C
authors.lastname: Wu
authors.forename: Weijuan
authors.initials: W
authors.lastname: Ma
authors.forename: Yongtao
authors.initials: Y
authors.lastname: Zhang
authors.forename: Tiezhou
authors.initials: T
authors.lastname: Hou
authors.forename: Honghai
authors.initials: H
authors.lastname: Xu
authors.forename: Shixun
authors.initials: S
authors.lastname: Wu
authors.forename: Xiao
authors.initials: X
authors.lastname: Yao
authors.forename: Xiong
authors.initials: X
authors.lastname: Guo
mesh_terms: D000368:Aged; D002358:Cartilage, Articular / Q000378:metabolism* / Q000473:pathology; D016022:Case-Control Studies; D002478:Cells, Cultured; D019902:Chondrocytes / Q000378:metabolism / Q000473:pathology; D015536:Down-Regulation / Q000502:physiology; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D005260:Female; D006801:Humans; D057767:Kashin-Beck Disease / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D017350:N-Acetylgalactosaminyltransferases / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D010003:Osteoarthritis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D051153:Wnt Proteins / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism; D000099249:Proteoglycan Link Protein
chemical_list: D016326:Extracellular Matrix Proteins; D017350:N-Acetylgalactosaminyltransferases; D011509:Proteoglycans; D012333:RNA, Messenger; D051153:Wnt Proteins; D051176:beta Catenin; D000099249:Proteoglycan Link Protein; C472559:chondroitin sulfate N-acetylgalactosaminyltransferase-1