Regulation of Anti-Inflammatory Gene Expression in Vascular Endothelial Cells by EPAC1Timothy M Palmer1 and Stephen J Yarwood2*
- *Corresponding Author:
- Stephen J Yarwood
Institute of Molecular, Cell and Systems Biology
College of Medical
Veterinary and Life Sciences
University of Glasgow
Glasgow G12 8QQ, United Kingdom
E-mail: [email protected]
Received date: September 16, 2015 Accepted date: September 18, 2015; Published date: September 23, 2015
Citation: Palmer TM, Yarwood SJ (2015) Regulation of Anti-Inflammatory Gene Expression in Vascular Endothelial Cells by EPAC1. J Cell Signal 1:103. doi:10.4172/jcs.1000103
Copyright: © 2015 Palmer TM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Suppressor of cytokine signalling 3 (SOCS3) is a potent inhibitor of pro-inflammatory pathways involved in atherogenesis and the development of neo-intimal hyperplasia (NIH), which contributes to the in-stent re-stenosis responsible for the failure of percutaneous coronary intervention (PCI) procedures. We have shown that cyclic AMP sensor EPAC1 triggers induction of the SOCS3 gene in vascular endothelial cells (VECs), thereby attenuating interleukin 6 (IL-6)-mediated pro-inflammatory signalling. We propose that EPAC1 localisation to the nuclear pore controls cyclic AMP-mediated activation of a C/EBPβ/c-Jun transcriptional complex, leading to SOCS3 induction and suppression of pro-inflammatory signalling. Future work in this area will involve an integrated approach to determine the wider significance of the EPAC1-C/EBPβ/c-Jun pathway in controlling human VEC function and identify new therapeutic targets for management of chronic inflammation in vascular settings.