Retinoid acid inhibits IL-1-induced iNOS, COX-2 and chemokine production in human chondrocytes
| العنوان: | Retinoid acid inhibits IL-1-induced iNOS, COX-2 and chemokine production in human chondrocytes |
|---|---|
| المؤلفون: | Leou Chyr Lin, Shyu Jye Wang, Ling-Jun Ho, Li Feng Hung, Chun Chin T. Liang, Jenn Haung Lai, Tsung Yun Hou, Deh-Ming Chang |
| المصدر: | Immunological investigations. 37(7) |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | medicine.medical_specialty, Chemokine, medicine.drug_class, MAP Kinase Kinase 4, medicine.medical_treatment, Immunology, Retinoic acid, Nitric Oxide Synthase Type II, Tretinoin, Biology, CCL8, Chondrocyte, Dinoprostone, Nitric oxide, Cell Line, chemistry.chemical_compound, Chondrocytes, Internal medicine, medicine, Humans, Retinoid, Anthracenes, General Medicine, Molecular biology, Nitric oxide synthase, Transcription Factor AP-1, Endocrinology, medicine.anatomical_structure, chemistry, Cyclooxygenase 2, biology.protein, Chemokines, Prostaglandin E, Interleukin-1 |
| الوصف: | This study aims to investigate the effects and mechanisms of all-trans retinoic acid (t-RA) on interleukin(IL)-1-induced production of several inflammatory mediators in human chondrocytes. The cartilage from OA patients receiving total knee or total hip replacement was obtained and chondrocytes were prepared. Chemokine concentrations were measured by ELISA. The expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was determined by Western blotting and/or RT/PCR. Nitrite levels were measured by Griess assays. The DNA-binding activity and transcriptional activity of activator protein-1 (AP-1) were measured by electrophoresis mobility shift assay and luciferase assay. We showed that t-RA suppressed IL-1-induced release of chemokines, including regulated upon activation, normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein 2 (MCP-2), macrophage inflammatory protein-1alpha (MIP-1alpha) and MIP-1beta. Four different retinoid derivatives all preserved inhibitory effects albeit the potency was different. t-RA potently suppressed IL-1-induced expression of iNOS and COX-2 and production of nitric oxide and prostaglandin E(2). In consistent with the results in primary chondrocytes, t-RA down-regulated IL-1-induced AP-1 DNA binding activity and transcriptional activity in a human fibroblast-like (commercially labeled as chondrocyte) cell line. By examining the effect of a c-jun N-terminal kinase (JNK) specific inhibitor, we showed that the suppression of JNK-AP-1 signaling was enough to inhibit IL-1-induced production of chemokines and activation of iNOS and COX-2 pathways. Collectively, our results raise a therapeutic option that intra-articular administration of retinoid derivatives at 10-1000 nanomolar concentrations may be effective to suppress the progression of inflammatory OA. |
| تدمد: | 1532-4311 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a63001b7124b222d6a1b992ff85aad60 https://pubmed.ncbi.nlm.nih.gov/18821215 |
| رقم الانضمام: | edsair.doi.dedup.....a63001b7124b222d6a1b992ff85aad60 |
| قاعدة البيانات: | OpenAIRE |
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