ArticleInternational orthopaedics2013
Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis.
Article in International orthopaedics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Quercetin Simultaneously Treats Skeletal Fluorosis and Kashin-Beck Disease by Modulating HIF-1 and Ferroptosis Signaling Pathways.Biological trace element research · 2025Article
- The Long-term Efficacy of Total Knee Arthroplasty on End-stage Kashin-Beck Disease of the Knee in Highland Tibetan Areas Patients: A Retrospective Study with 10-Year Follow-up.Orthopaedic surgery · 2024Article
- Hyaluronan and Proteoglycan Link Protein 1 Activates the BMP4/Smad1/5/8 Signaling Pathway to Promote Osteogenic Differentiation: an Implication in Fracture Healing.Molecular biotechnology · 2023Article
- Detection of selenoprotein transcriptome in chondrocytes of patients with Kashin-Beck disease.Frontiers in cell and developmental biology · 2023Article
- HAPLN1 Affects Cell Viability and Promotes the Pro-Inflammatory Phenotype of Fibroblast-Like Synoviocytes.Frontiers in immunology · 2022Article
- Article
- Comparison of the major cell populations among osteoarthritis, Kashin-Beck disease and healthy chondrocytes by single-cell RNA-seq analysis.Cell death & disease · 2021Article
- Proteome Alterations in Equine Osteochondrotic Chondrocytes.International journal of molecular sciences · 2019Article
- Biological Analysis of Gene Expression and Clinical Variables Suggest FZD1 as a Novel Biomarker for Patients with Kashin-Beck Disease, an Endemic Osteoarthritis in China.Disease markers · 2019Article
- microRNA-140 Inhibits Inflammation and Stimulates Chondrogenesis in a Model of Interleukin 1β-induced Osteoarthritis.Molecular therapy. Nucleic acids · 2016Article
- Copper, iron, and selenium dietary deficiencies negatively impact skeletal integrity: A review.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- An integrative systems genetics approach reveals potential causal genes and pathways related to obesity.Genome medicine · 2015Article
- Gene expression signature in endemic osteoarthritis by microarray analysis.International journal of molecular sciences · 2015Article
- Transcriptome-wide analysis of messenger RNA decay in normal and osteoarthritic human articular chondrocytes.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Total knee arthroplasty in elderly patients with severe Kashin-Beck disease of the knee.International orthopaedics · 2014Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeKashin-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.
methodsAgilent 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.
resultsCSGalNAcT-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.
conclusionsThe 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.
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