ArticleBiochemical pharmacology2010
Transcriptional and post-transcriptional regulation of iNOS expression in human chondrocytes.
Article in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 63 citations in OpenAlex.
- Targeting of CIRP attenuates osteoarthritis progression via suppressing TLR4/NF‑κB/NLRP3 signaling axis.International journal of molecular medicine · 2026Article
- Ginkgetin delays the progression of osteoarthritis by inhibiting the NF-κB and MAPK signaling pathways.Journal of orthopaedic surgery and research · 2025Article
- The macrocyclic lactone oxacyclododecindione reduces fibrosis progression.Frontiers in pharmacology · 2023Article
- Drug Candidates for Autoimmune Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Curvularin Isolated FromFrontiers in microbiology · 2022Article
- Role of iNOS in osteoarthritis: Pathological and therapeutic aspects.Journal of cellular physiology · 2020Review
- Imperatorin suppresses IL-1β-induced iNOS expression via inhibiting ERK-MAPK/AP1 signaling in primary human OA chondrocytes.International immunopharmacology · 2020Article
- Control of cytokine mRNA degradation by the histone deacetylase inhibitor ITF2357 in rheumatoid arthritis fibroblast-like synoviocytes: beyond transcriptional regulation.Arthritis research & therapy · 2018Article
- Anti-inflammatory activities of Guang-Pheretima extract in lipopolysaccharide-stimulated RAW 264.7 murine macrophages.BMC complementary and alternative medicine · 2018Article
- SETD1B Activates iNOS Expression in Myeloid-Derived Suppressor Cells.Cancer research · 2017Article
- Reconstitution of T Cell Proliferation under Arginine Limitation: Activated Human T Cells Take Up CitrullineFrontiers in immunology · 2017Article
- Dihydrotanshinone-I interferes with the RNA-binding activity of HuR affecting its post-transcriptional function.Scientific reports · 2015Article
- The NF-κB p65 and p50 homodimer cooperate with IRF8 to activate iNOS transcription.BMC cancer · 2015Article
- Article
- Transcriptome-wide analysis of messenger RNA decay in normal and osteoarthritic human articular chondrocytes.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Endothelial dysfunction in tristetraprolin-deficient mice is not caused by enhanced tumor necrosis factor-α expression.The Journal of biological chemistry · 2014Article
- Converging pathways involving microRNA-206 and the RNA-binding protein KSRP control post-transcriptionally utrophin A expression in skeletal muscle.Nucleic acids research · 2014Article
- Role of KSRP in control of type I interferon and cytokine expression.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Artichoke, cynarin and cyanidin downregulate the expression of inducible nitric oxide synthase in human coronary smooth muscle cells.Molecules (Basel, Switzerland) · 2014Article
- Nitric oxide synthase: non-canonical expression patterns.Frontiers in immunology · 2014Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Chondrocytes are important for the development and maintenance of articular cartilage. However, both in osteoarthritis (OA) and rheumatoid arthritis (RA) chondrocytes are involved in the process of cartilage degradation and synthesize important immunomodulatory mediators, including nitric oxide (NO) generated by the inducible NO synthase (iNOS). To uncover the role of iNOS in the pathomechanisms of OA and RA, we analyzed the regulation of iNOS expression using immortalized human chondrocytes as a reproducible model. In C-28/I2 chondrocytes, iNOS expression was associated with the expression of the chondrocyte phenotype. Peak induction by a cytokine cocktail occurred between 6 and 8h and declined by 24h. Inhibition of p38MAPK, NF-kappaB and the JAK2-STAT-1alpha pathways resulted in a reduction of iNOS expression. In contrast to other cell types, the cytokine-mediated induction of the human iNOS promoter paralleled the induction rate of the iNOS mRNA expression in C-28/I2 chondrocytes. However, in addition post-transcriptional regulation of iNOS expression by the RNA binding protein KSRP seems to operate in these cells. As seen in other chondrocyte models, glucocorticoids were not able to inhibit cytokine-induced iNOS expression in C-28/I2 cells, due to the lack of the glucocorticoid receptor mRNA expression. In this model of glucocorticoid-resistance, the new fungal anti-inflammatory compound S-curvularin was able to inhibit cytokine-induced iNOS expression and iNOS-dependent NO-production. In summary, we demonstrate for the first time that differentiated human immortalized C-28/I2 chondrocytes are a representative cell culture model to investigate iNOS gene expression in human joint diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.