<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16(6)</volume><submitter>Yulia A</submitter><funding>Action Medical Research</funding><funding>Borne</funding><funding>National Institute for Health Research Biomedical Research Centre</funding><pubmed_abstract>Previously, we showed that cAMP increased COX-2 expression in myometrial cells via MAPK. Here, we have extended these observations, using primary myometrial cell cultures to show that the cAMP agonist, forskolin, enhances IL-1β-driven COX-2 expression. We then explored the role of A-kinase interacting protein (AKIP1), which modulates the effect of PKA on p65 activation. AKIP1 knockdown reversed the effect of forskolin, such that its addition inhibited IL-1β-induced COX-2 mRNA expression and reduced the IL-1β-induced increase in nuclear levels of p65 and c-jun. Forskolin alone and with IL-1β increased IκBα mRNA expression suggesting that in the context of inflammation and in the presence of AKIP1, cAMP enhances p65 activation. AKIP1 knockdown reversed these changes. Interestingly, AKIP1 kno</pubmed_abstract><journal>PloS one</journal><pagination>e0252720</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8224895</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>PKA and AKIP1 interact to mediate cAMP-driven COX-2 expression: A potentially pivotal interaction in preterm and term labour.</pubmed_title><pmcid>PMC8224895</pmcid><pubmed_authors>Johnson MR</pubmed_authors><pubmed_authors>Lei K</pubmed_authors><pubmed_authors>Singh N</pubmed_authors><pubmed_authors>Varley AJ</pubmed_authors><pubmed_authors>Sooranna SR</pubmed_authors><pubmed_authors>Yulia A</pubmed_authors><pubmed_authors>Markovic D</pubmed_authors></additional><is_claimable>false</is_claimable><name>PKA and AKIP1 interact to mediate cAMP-driven COX-2 expression: A potentially pivotal interaction in preterm and term labour.</name><description>Previously, we showed that cAMP increased COX-2 expression in myometrial cells via MAPK. Here, we have extended these observations, using primary myometrial cell cultures to show that the cAMP agonist, forskolin, enhances IL-1β-driven COX-2 expression. We then explored the role of A-kinase interacting protein (AKIP1), which modulates the effect of PKA on p65 activation. AKIP1 knockdown reversed the effect of forskolin, such that its addition inhibited IL-1β-induced COX-2 mRNA expression and reduced the IL-1β-induced increase in nuclear levels of p65 and c-jun. Forskolin alone and with IL-1β increased IκBα mRNA expression suggesting that in the context of inflammation and in the presence of AKIP1, cAMP enhances p65 activation. AKIP1 knockdown reversed these changes. Interestingly, AKIP1 kno</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2026-05-08T00:24:38.791Z</modification><creation>2022-02-10T21:17:25.138Z</creation></dates><accession>S-EPMC8224895</accession><cross_references><pubmed>34166397</pubmed><doi>10.1371/journal.pone.0252720</doi></cross_references></HashMap>