We are analyzing https://link.springer.com/article/10.1186/s13075-014-0484-2.

Title:
UDP-glucose dehydrogenase modulates proteoglycan synthesis in articular chondrocytes: its possible involvement and regulation in osteoarthritis | Arthritis Research & Therapy
Description:
Introduction The objective of this study was to investigate the possible role of UDP-glucose dehydrogenase (UGDH) in osteoarthritis (OA) and uncover whether, furthermore how interleukin-1beta (IL-1β) affects UGDH gene expression. Methods UGDH specific siRNAs were applied to determine the role of UGDH in proteoglycan (PG) synthesis in human articular chondrocytes. Protein levels of UGDH and Sp1 in human and rat OA cartilage were detected. Then, human primary chondrocytes were treated with IL-1β to find out whether and how IL-1β could regulate the gene expression of UGDH and its trans-regulators, that is Sp1, Sp3 and c-Krox. Finally, p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 and stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) inhibitor SP600125 were used to pick out the pathway that mediated the IL-1β-modulated PGs synthesis and gene expression of UGDH, Sp1, Sp3 and c-Krox. Results UGDH specific siRNAs markedly inhibited UGDH mRNA and protein expression, and thus led to an obvious suppression of PGs synthesis in human articular chondrocytes. UGDH protein level in human and rat OA cartilage were much lower than the corresponding controls and negatively correlated to the degree of OA. Decrease in Sp1 protein level was also observed in human and rat OA cartilage respectively. Meanwhile, IL-1β suppressed UGDH gene expression in human articular chondrocytes in the late phase, which also modulated gene expression of Sp1, Sp3 and c-Krox and increased both Sp3/Sp1 and c-Krox/Sp1 ratio. Moreover, the inhibition of SAP/JNK and p38 MAPK pathways both resulted in an obvious attenuation of the IL-1β-induced suppression on the UGDH gene expression. Conclusions UGDH is essential in the PGs synthesis of articular chondrocytes, while the suppressed expression of UGDH might probably be involved in advanced OA, partly due to the modulation of p38 MAPK and SAP/JNK pathways and its trans-regulators by IL-1β.
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Keywords {🔍}

ugdh, cartilage, chondrocytes, protein, ilβ, expression, human, gene, articular, pubmed, figure, article, synthesis, google, scholar, level, cas, gag, ckrox, dehydrogenase, mapk, udpglucose, sapjnk, rat, treated, mrna, content, osteoarthritis, study, detected, activity, minutes, file, authors, chondrocyte, control, usa, assay, mankin, additional, data, role, pgs, observed, pathogenesis, ngml, wang, transregulators, pathway, ratio,

Topics {✒️}

transforming growth factor-beta real-time pcr key pro-inflammatory cytokine udp-glucose dehydrogenase expression human udp-glucose 6-dehydrogenase functional udp-glucose dehydrogenase article download pdf il-1β-modulated pgs synthesis osteo-arthritic human hips serum-free dmem/f-12 il-1β-induced pg loss exogenous il-1β failed wilcoxon rank-sum test national research council stimuli including 17β-oestradiol full access caffeine-induced fetal rat specialized research fund western blotting assay human recombinant il-1β mid-zone highly synthesize nf-κb signaling udp-glucose dehydrogenase 10 ng/ml il-1β anti-phospho-sapk/jnk inhibits gene transcription c-krox mrna levels prostate cancer cells related subjects connect tissue res il-1β-induced suppression anti-phospho-p38 mapk c-krox/sp1 ratio interleukin 1beta pathway rt-pcr assay represses sp1-mediated activation proteoglycans rt-pcr modulated gene expression privacy choices/manage cookies il-1β modulated downstream cascade reaction sp1-mediated transcriptional activation stimulated cartilage degeneration modulating ugdh trans-regulators time-dependent manner osteoarthritic human chondrocytes c-krox mediated modulate hyaluronan production c-krox gene gene transcription due

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         headline:UDP-glucose dehydrogenase modulates proteoglycan synthesis in articular chondrocytes: its possible involvement and regulation in osteoarthritis
         description:The objective of this study was to investigate the possible role of UDP-glucose dehydrogenase (UGDH) in osteoarthritis (OA) and uncover whether, furthermore how interleukin-1beta (IL-1β) affects UGDH gene expression. UGDH specific siRNAs were applied to determine the role of UGDH in proteoglycan (PG) synthesis in human articular chondrocytes. Protein levels of UGDH and Sp1 in human and rat OA cartilage were detected. Then, human primary chondrocytes were treated with IL-1β to find out whether and how IL-1β could regulate the gene expression of UGDH and its trans-regulators, that is Sp1, Sp3 and c-Krox. Finally, p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 and stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) inhibitor SP600125 were used to pick out the pathway that mediated the IL-1β-modulated PGs synthesis and gene expression of UGDH, Sp1, Sp3 and c-Krox. UGDH specific siRNAs markedly inhibited UGDH mRNA and protein expression, and thus led to an obvious suppression of PGs synthesis in human articular chondrocytes. UGDH protein level in human and rat OA cartilage were much lower than the corresponding controls and negatively correlated to the degree of OA. Decrease in Sp1 protein level was also observed in human and rat OA cartilage respectively. Meanwhile, IL-1β suppressed UGDH gene expression in human articular chondrocytes in the late phase, which also modulated gene expression of Sp1, Sp3 and c-Krox and increased both Sp3/Sp1 and c-Krox/Sp1 ratio. Moreover, the inhibition of SAP/JNK and p38 MAPK pathways both resulted in an obvious attenuation of the IL-1β-induced suppression on the UGDH gene expression. UGDH is essential in the PGs synthesis of articular chondrocytes, while the suppressed expression of UGDH might probably be involved in advanced OA, partly due to the modulation of p38 MAPK and SAP/JNK pathways and its trans-regulators by IL-1β.
         datePublished:2014-12-03T00:00:00Z
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            Mankin Score
            Cartilage Homeostasis
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            Rheumatology
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      headline:UDP-glucose dehydrogenase modulates proteoglycan synthesis in articular chondrocytes: its possible involvement and regulation in osteoarthritis
      description:The objective of this study was to investigate the possible role of UDP-glucose dehydrogenase (UGDH) in osteoarthritis (OA) and uncover whether, furthermore how interleukin-1beta (IL-1β) affects UGDH gene expression. UGDH specific siRNAs were applied to determine the role of UGDH in proteoglycan (PG) synthesis in human articular chondrocytes. Protein levels of UGDH and Sp1 in human and rat OA cartilage were detected. Then, human primary chondrocytes were treated with IL-1β to find out whether and how IL-1β could regulate the gene expression of UGDH and its trans-regulators, that is Sp1, Sp3 and c-Krox. Finally, p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 and stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) inhibitor SP600125 were used to pick out the pathway that mediated the IL-1β-modulated PGs synthesis and gene expression of UGDH, Sp1, Sp3 and c-Krox. UGDH specific siRNAs markedly inhibited UGDH mRNA and protein expression, and thus led to an obvious suppression of PGs synthesis in human articular chondrocytes. UGDH protein level in human and rat OA cartilage were much lower than the corresponding controls and negatively correlated to the degree of OA. Decrease in Sp1 protein level was also observed in human and rat OA cartilage respectively. Meanwhile, IL-1β suppressed UGDH gene expression in human articular chondrocytes in the late phase, which also modulated gene expression of Sp1, Sp3 and c-Krox and increased both Sp3/Sp1 and c-Krox/Sp1 ratio. Moreover, the inhibition of SAP/JNK and p38 MAPK pathways both resulted in an obvious attenuation of the IL-1β-induced suppression on the UGDH gene expression. UGDH is essential in the PGs synthesis of articular chondrocytes, while the suppressed expression of UGDH might probably be involved in advanced OA, partly due to the modulation of p38 MAPK and SAP/JNK pathways and its trans-regulators by IL-1β.
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         Mankin Score
         Cartilage Homeostasis
         Degenerative Cartilage
         Rheumatology
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      name:Faculté de Médecine, UMR 7365 CNRS-Nancy Université, Vandoeuvre-lès-Nancy, France
      name:Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Faculté de Médecine, UMR 7365 CNRS-Nancy Université, Vandoeuvre-lès-Nancy, France
      name:Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China
      name:Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China
      name:Department of pharmacology, School of Basic Medical Science, Wuhan University, Wuhan, China
      name:Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China

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