Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR
OxLDL is recognized by macrophage scavenger receptors, including CD36; we have recently found that Platelet-Activating Factor Receptor (PAFR) is also involved. Since PAFR in macrophages is associated with suppressor function, we examined the effect of oxLDL on macrophage phenotype. It was found that...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/198193 |
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| author | Francisco J. Rios Marianna M. Koga Mateus Pecenin Matheus Ferracini Magnus Gidlund S. Jancar |
| author_facet | Francisco J. Rios Marianna M. Koga Mateus Pecenin Matheus Ferracini Magnus Gidlund S. Jancar |
| author_sort | Francisco J. Rios |
| collection | DOAJ |
| description | OxLDL is recognized by macrophage scavenger receptors, including CD36; we have recently found that Platelet-Activating Factor Receptor (PAFR) is also involved. Since PAFR in macrophages is associated with suppressor function, we examined the effect of oxLDL on macrophage phenotype. It was found that the presence of oxLDL during macrophage differentiation induced high mRNA levels to IL-10, mannose receptor, PPARγ and arginase-1 and low levels of IL-12 and iNOS. When human THP-1 macrophages were pre-treated with oxLDL then stimulated with LPS, the production of IL-10 and TGF-β significantly increased, whereas that of IL-6 and IL-8 decreased. In murine TG-elicited macrophages, this protocol significantly reduced NO, iNOS and COX2 expression. Thus, oxLDL induced macrophage differentiation and activation towards the alternatively activated M2-phenotype. In murine macrophages, oxLDL induced TGF-β, arginase-1 and IL-10 mRNA expression, which were significantly reduced by pre-treatment with PAFR antagonists (WEB and CV) or with antibodies to CD36. The mRNA expression of IL-12, RANTES and CXCL2 were not affected. We showed that this profile of macrophage activation is dependent on the engagement of both CD36 and PAFR. We conclude that oxLDL induces alternative macrophage activation by mechanisms involving CD36 and PAFR. |
| format | Article |
| id | doaj-art-4ce27a77be7944f9b2d6a3cb4c156aaa |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4ce27a77be7944f9b2d6a3cb4c156aaa2025-02-03T01:00:53ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/198193198193Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFRFrancisco J. Rios0Marianna M. Koga1Mateus Pecenin2Matheus Ferracini3Magnus Gidlund4S. Jancar5Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Avenida Professor Lineu Prestes 1730, ICB IV—Sala 140/146, 05508-900 Sao Paulo, SP, BrazilDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Avenida Professor Lineu Prestes 1730, ICB IV—Sala 140/146, 05508-900 Sao Paulo, SP, BrazilDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Avenida Professor Lineu Prestes 1730, ICB IV—Sala 140/146, 05508-900 Sao Paulo, SP, BrazilDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Avenida Professor Lineu Prestes 1730, ICB IV—Sala 140/146, 05508-900 Sao Paulo, SP, BrazilDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Avenida Professor Lineu Prestes 1730, ICB IV—Sala 140/146, 05508-900 Sao Paulo, SP, BrazilDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Avenida Professor Lineu Prestes 1730, ICB IV—Sala 140/146, 05508-900 Sao Paulo, SP, BrazilOxLDL is recognized by macrophage scavenger receptors, including CD36; we have recently found that Platelet-Activating Factor Receptor (PAFR) is also involved. Since PAFR in macrophages is associated with suppressor function, we examined the effect of oxLDL on macrophage phenotype. It was found that the presence of oxLDL during macrophage differentiation induced high mRNA levels to IL-10, mannose receptor, PPARγ and arginase-1 and low levels of IL-12 and iNOS. When human THP-1 macrophages were pre-treated with oxLDL then stimulated with LPS, the production of IL-10 and TGF-β significantly increased, whereas that of IL-6 and IL-8 decreased. In murine TG-elicited macrophages, this protocol significantly reduced NO, iNOS and COX2 expression. Thus, oxLDL induced macrophage differentiation and activation towards the alternatively activated M2-phenotype. In murine macrophages, oxLDL induced TGF-β, arginase-1 and IL-10 mRNA expression, which were significantly reduced by pre-treatment with PAFR antagonists (WEB and CV) or with antibodies to CD36. The mRNA expression of IL-12, RANTES and CXCL2 were not affected. We showed that this profile of macrophage activation is dependent on the engagement of both CD36 and PAFR. We conclude that oxLDL induces alternative macrophage activation by mechanisms involving CD36 and PAFR.http://dx.doi.org/10.1155/2013/198193 |
| spellingShingle | Francisco J. Rios Marianna M. Koga Mateus Pecenin Matheus Ferracini Magnus Gidlund S. Jancar Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR Mediators of Inflammation |
| title | Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR |
| title_full | Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR |
| title_fullStr | Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR |
| title_full_unstemmed | Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR |
| title_short | Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR |
| title_sort | oxidized ldl induces alternative macrophage phenotype through activation of cd36 and pafr |
| url | http://dx.doi.org/10.1155/2013/198193 |
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