Regulation of anti-inflammatory gene expression in vascular endothelial cells by EPAC1

Timothy M. Palmer, Stephen J Yarwood

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Abstract

Suppressor of cytokine signalling 3 (SOCS3) is a potent inhibitor of pro-inflammatory pathways involved inatherogenesis and the development of neo-intimal hyperplasia (NIH), which contributes to the in-stent re-stenosisresponsible for the failure of percutaneous coronary intervention (PCI) procedures. We have shown that cyclic AMPsensor EPAC1 triggers induction of the SOCS3 gene in vascular endothelial cells (VECs), thereby attenuatinginterleukin 6 (IL-6)-mediated pro-inflammatory signalling. We propose that EPAC1 localisation to the nuclear porecontrols cyclic AMP-mediated activation of a C/EBPβ/c-Jun transcriptional complex, leading to SOCS3 induction andsuppression of pro-inflammatory signalling. Future work in this area will involve an integrated approach to determinethe wider significance of the EPAC1-C/EBPβ/c-Jun pathway in controlling human VEC function and identify newtherapeutic targets for management of chronic inflammation in vascular settings.
Original languageEnglish
Article number1000103
JournalJournal of Cell Signaling
Volume1
Issue number1
DOIs
Publication statusPublished - 9 Nov 2015

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