Table of Contents Author Guidelines Submit a Manuscript
International Journal of Inflammation
Volume 2015 (2015), Article ID 201571, 10 pages
Research Article

CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2

Département de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada J1K 2R1

Received 22 August 2015; Revised 5 November 2015; Accepted 8 November 2015

Academic Editor: G. Rogler

Copyright © 2015 Bérengère Tanné et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cell migration via chemokine receptor CCR7 expression is an essential function of the immune system. We previously showed that prostaglandin (PG), an important immunomodulatory molecule, increases CCR7 expression and function in monocytes. Here, we explore the role of the liver X receptor α (LXRα) activation on CCR7 expression in Mono-Mac-1 (MM-1) cells in the presence of PG. To do this, MM-1 cells were stimulated with the LXRα synthetic agonist T0901317 in the presence or absence of PG. CCR7 mRNA transcription was measured using quantitative RT-PCR and protein expression was examined using flow cytometry. CCR7 function was analyzed using migration assays in response to CCL19/CCL21, which are natural ligands for CCR7. Our results show that agonist-mediated activation of LXRα in the presence of PG increases CCR7 mRNA transcription and MM-1 cell migratory capacity in response to CCL19/21. In addition, our results demonstrate that engagement of the E-prostanoids 2 and 4 (E/E) receptors present on MM-1 cells is responsible for the observed increase in CCR7 mRNA expression and function during LXRα activation. Examination of monocyte migration in response to lipid derivatives such as PG and oxysterols that are produced at sites of chronic inflammation would contribute to understanding the excessive monocyte migration that characterizes atherosclerosis.