<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Nakano R</submitter><pubmed_abstract>The pro-inflammatory cytokine interleukin 1&lt;i>β&lt;/i> (IL-1&lt;i>β&lt;/i>) induces the synthesis of prostaglandin E&lt;sub>2&lt;/sub> by upregulating cyclooxygenase-2 (COX-2) in the synovial tissue of individuals with autoimmune diseases, such as rheumatoid arthritis (RA). IL-1&lt;i>β&lt;/i>-mediated stimulation of NF-&lt;i>κ&lt;/i>B and MAPK signaling is important for the pathogenesis of RA; however, crosstalk(s) between NF-&lt;i>κ&lt;/i>B and MAPK signaling remains to be understood. In this study, we established a model for IL-1&lt;i>β&lt;/i>-induced synovitis and investigated the role of NF-&lt;i>κ&lt;/i>B and MAPK signaling in synovitis. We observed an increase in the mRNA and protein levels of COX-2 and prostaglandin E&lt;sub>2&lt;/sub> release in cells treated with IL-1&lt;i>β&lt;/i>. NF-&lt;i>κ&lt;/i>B and ERK1/2 inhibitors significantly reduc</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>579266</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7576893</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Non-Transcriptional and Translational Function of Canonical NF-&lt;i>κ&lt;/i>B Signaling in Activating ERK1/2 in IL-1&lt;i>β&lt;/i>-Induced COX-2 Expression in Synovial Fibroblasts.</pubmed_title><pmcid>PMC7576893</pmcid><pubmed_authors>Kitanaka T</pubmed_authors><pubmed_authors>Konno T</pubmed_authors><pubmed_authors>Yamazaki J</pubmed_authors><pubmed_authors>Nakayama T</pubmed_authors><pubmed_authors>Nakano R</pubmed_authors><pubmed_authors>Namba S</pubmed_authors><pubmed_authors>Suwabe Y</pubmed_authors><pubmed_authors>Sugiya H</pubmed_authors><pubmed_authors>Kitanaka N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Non-Transcriptional and Translational Function of Canonical NF-&lt;i>κ&lt;/i>B Signaling in Activating ERK1/2 in IL-1&lt;i>β&lt;/i>-Induced COX-2 Expression in Synovial Fibroblasts.</name><description>The pro-inflammatory cytokine interleukin 1&lt;i>β&lt;/i> (IL-1&lt;i>β&lt;/i>) induces the synthesis of prostaglandin E&lt;sub>2&lt;/sub> by upregulating cyclooxygenase-2 (COX-2) in the synovial tissue of individuals with autoimmune diseases, such as rheumatoid arthritis (RA). IL-1&lt;i>β&lt;/i>-mediated stimulation of NF-&lt;i>κ&lt;/i>B and MAPK signaling is important for the pathogenesis of RA; however, crosstalk(s) between NF-&lt;i>κ&lt;/i>B and MAPK signaling remains to be understood. In this study, we established a model for IL-1&lt;i>β&lt;/i>-induced synovitis and investigated the role of NF-&lt;i>κ&lt;/i>B and MAPK signaling in synovitis. We observed an increase in the mRNA and protein levels of COX-2 and prostaglandin E&lt;sub>2&lt;/sub> release in cells treated with IL-1&lt;i>β&lt;/i>. NF-&lt;i>κ&lt;/i>B and ERK1/2 inhibitors significantly reduc</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2026-04-14T23:19:29.903Z</modification><creation>2020-10-30T08:34:43Z</creation></dates><accession>S-EPMC7576893</accession><cross_references><pubmed>33117381</pubmed><doi>10.3389/fimmu.2020.579266</doi></cross_references></HashMap>