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Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis.
Int Orthop. 2013 Oct; 37(10):2051-9.IO

Abstract

PURPOSE

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+Show Affiliations

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.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23748413

Citation

Zheng, Jingjing, et al. "Abnormal Expression of Chondroitin Sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in Cartilage With Kashin-Beck Disease and Primary Osteoarthritis." International Orthopaedics, vol. 37, no. 10, 2013, pp. 2051-9.
Zheng J, Wu C, Ma W, et al. Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis. Int Orthop. 2013;37(10):2051-9.
Zheng, J., Wu, C., Ma, W., Zhang, Y., Hou, T., Xu, H., Wu, S., Yao, X., & Guo, X. (2013). Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis. International Orthopaedics, 37(10), 2051-9. https://doi.org/10.1007/s00264-013-1937-y
Zheng J, et al. Abnormal Expression of Chondroitin Sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in Cartilage With Kashin-Beck Disease and Primary Osteoarthritis. Int Orthop. 2013;37(10):2051-9. PubMed PMID: 23748413.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis. AU - Zheng,Jingjing, AU - Wu,Cuiyan, AU - Ma,Weijuan, AU - Zhang,Yongtao, AU - Hou,Tiezhou, AU - Xu,Honghai, AU - Wu,Shixun, AU - Yao,Xiao, AU - Guo,Xiong, Y1 - 2013/06/08/ PY - 2013/04/16/received PY - 2013/05/10/accepted PY - 2013/6/11/entrez PY - 2013/6/12/pubmed PY - 2014/6/3/medline SP - 2051 EP - 9 JF - International orthopaedics JO - Int Orthop VL - 37 IS - 10 N2 - PURPOSE: 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. SN - 1432-5195 UR - https://www.unboundmedicine.com/medline/citation/23748413/Abnormal_expression_of_chondroitin_sulphate_N_acetylgalactosaminyltransferase_1_and_Hapln_1_in_cartilage_with_Kashin_Beck_disease_and_primary_osteoarthritis_ L2 - https://dx.doi.org/10.1007/s00264-013-1937-y DB - PRIME DP - Unbound Medicine ER -