Prostaglandin E2Does Not Modulate CCR7 Expression and Functionality after Differentiation of Blood Monocytes into Macrophages
| Autor: | Nancy Dumais, Marc-André Allaire, Bérengère Tanné, Sandra C. Côté |
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| Rok vydání: | 2013 |
| Předmět: |
Article Subject
chemical and pharmacologic phenomena C-C chemokine receptor type 7 03 medical and health sciences Chemokine receptor 0302 clinical medicine immune system diseases lcsh:Pathology Immunology and Allergy Medicine Macrophage Prostaglandin E2 030304 developmental biology 0303 health sciences business.industry CCL19 hemic and immune systems Chemotaxis biological factors Cell biology Monocyte differentiation Immunology lipids (amino acids peptides and proteins) business lcsh:RB1-214 Research Article 030215 immunology medicine.drug CCL21 |
| Zdroj: | International Journal of Inflammation International Journal of Inflammation, Vol 2013 (2013) |
| ISSN: | 2042-0099 2090-8040 |
| Popis: | Previously, we demonstrated that prostaglandin E2(PGE2) induces C-C chemokine receptor type 7 (CCR7) expression on human monocytes, which stimulates their subsequent migration in response to the CCR7 natural ligands CCL19 and CCL21. In this study, we determined whether PGE2affects CCR7 expression on macrophages. Flow cytometric analysis and chemotaxis assays were performed on Mono Mac-1-derived macrophage (MDMM-1) as well as unpolarized monocyte-derived macrophages (MDMs) to determine the CCR7 expression and functionality in the presence of PGE2. Data revealed that a MDMM-1 exhibited markedly downregulated CCR7 expression and functionality that were partially restored by treatment with PGE2. In MDMs, we observed a drastic downregulation of CCR7 expression and functionality that were unaffected following PGE2treatment. Our data indicate that monocyte differentiation induces the loss of CCR7 expression and that PGE2is unable to modulate CCR7 expression and functionality as shown previously in monocytes. |
| Databáze: | OpenAIRE |
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