ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016
Regulation of a disintegrins and metalloproteinase with thrombospondin motifs 7 during inflammation in nucleus pulposus (NP) cells: role of AP-1, Sp1 and NF-κB signaling.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Cytokine Imbalance as a Biomarker of Intervertebral Disk Degeneration.International journal of molecular sciences · 2023Review
- The Proteolysis of ECM in Intervertebral Disc Degeneration.International journal of molecular sciences · 2022Review
- Nicotinamide Phosphoribosyl Transferase Controls NLRP3 Inflammasome Activity Through MAPK and NF-κB Signaling in Nucleus Pulposus Cells, as Suppressed by Melatonin.Inflammation · 2020Article
- Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway.Disease markers · 2018Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe objective of this study is to explore the effect of inflammatory cytokines on a disintegrins and metalloproteinase with thrombospondin motifs 7 (ADAMTS7) and to demonstrate the role of Sp1, AP-1 and NF-κB signaling on the ADAMTS7 regulation during inflammation in NP cells.
methodsReal-time PCR was to detect the effect of ADAMTS7 knockdown on the expression of catabolic enzymes during inflammatory condition in NP cells. Real-time PCR, western blot, immunofluorescence and transfection experiments were used to observe the effect of tumor necrosis factor-α (TNF-α) or interleukin-1β on the expression and the activity of ADAMTS7, and demonstrated the role to Sp1, AP-1 and NF-κB in the regulation of ADAMTS7 during inflammation.
resultsAs other cells, ADAMTS7 knockdown suppressed the mRNA expression of catabolic factors during inflammation in human NP cells. However, the expression of ADAMTS7 mRNA and protein and the activity of ADAMTS7 promoter were refractory to inflammatory cytokines. In addition, Sp1, AP-1, not NF-κB signaling sustained the expression of ADAMTS7 mRNA, protein, as well as promoter activity during inflammation in NP cells.
conclusionADAMTS7 played a crucial role in the expression of catabolic genes in the presence of TNF-α and AP-1, Sp1, not NF-κB signaling were critical for the maintenance of ADAMTS7 expression during inflammation in NP cells.
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