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Cell migration via chemokine receptor CCR7 expression is an essential function of the immune system. We previously showed that prostaglandin E 2  (PGE 2 ), an important immunomodulatory molecule, increases CCR7 expression and function in monocytes. Here, we explore the role of the liver X receptor  α  (LXR α ) activation on CCR7 expression in Mono-Mac-1 (MM-1) cells in the presence of PGE 2 . To do this, MM-1 cells were stimulated with the LXR α  synthetic agonist T0901317 in the presence or absence of PGE 2 .  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 LXR α  in the presence of PGE 2  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 (EP 2 /EP 4 ) receptors present on MM-1 cells is responsible for the observed increase in  CCR7  mRNA expression and function during LXR α  activation. Examination of monocyte migration in response to lipid derivatives such as PGE 2  and oxysterols that are produced at sites of chronic inflammation would contribute to understanding the excessive monocyte migration that characterizes atherosclerosis.

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

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