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

Cell migration via chemokine receptor CCR7 expression is an essential function of the immune system. We previously showed that prostaglandin E2 (PGE2), an important immunomodulatory molecule, increases CCR7 expression and function in monocytes. Here, we explore the role of the liver X receptor α (LX...

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Main Authors: Bérengère Tanné, Stéphane Bernier, Nancy Dumais
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:International Journal of Inflammation
Online Access:http://dx.doi.org/10.1155/2015/201571
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author Bérengère Tanné
Stéphane Bernier
Nancy Dumais
author_facet Bérengère Tanné
Stéphane Bernier
Nancy Dumais
author_sort Bérengère Tanné
collection DOAJ
description Cell migration via chemokine receptor CCR7 expression is an essential function of the immune system. We previously showed that prostaglandin E2 (PGE2), 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 PGE2. To do this, MM-1 cells were stimulated with the LXRα synthetic agonist T0901317 in the presence or absence of PGE2. 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 PGE2 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 (EP2/EP4) 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 PGE2 and oxysterols that are produced at sites of chronic inflammation would contribute to understanding the excessive monocyte migration that characterizes atherosclerosis.
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series International Journal of Inflammation
spelling doaj-art-14b53f9fb2094a9eab7a92e18cefcd202025-08-20T03:54:29ZengWileyInternational Journal of Inflammation2090-80402042-00992015-01-01201510.1155/2015/201571201571CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2Bérengère Tanné0Stéphane Bernier1Nancy Dumais2Département de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, QC, J1K 2R1, CanadaDépartement de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, QC, J1K 2R1, CanadaDépartement de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, QC, J1K 2R1, CanadaCell migration via chemokine receptor CCR7 expression is an essential function of the immune system. We previously showed that prostaglandin E2 (PGE2), 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 PGE2. To do this, MM-1 cells were stimulated with the LXRα synthetic agonist T0901317 in the presence or absence of PGE2. 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 PGE2 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 (EP2/EP4) 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 PGE2 and oxysterols that are produced at sites of chronic inflammation would contribute to understanding the excessive monocyte migration that characterizes atherosclerosis.http://dx.doi.org/10.1155/2015/201571
spellingShingle Bérengère Tanné
Stéphane Bernier
Nancy Dumais
CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2
International Journal of Inflammation
title CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2
title_full CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2
title_fullStr CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2
title_full_unstemmed CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2
title_short CCR7 Receptor Expression in Mono-MAC-1 Cells: Modulation by Liver X Receptor α Activation and Prostaglandin E2
title_sort ccr7 receptor expression in mono mac 1 cells modulation by liver x receptor α activation and prostaglandin e2
url http://dx.doi.org/10.1155/2015/201571
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AT nancydumais ccr7receptorexpressioninmonomac1cellsmodulationbyliverxreceptoraactivationandprostaglandine2