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CXCL4 downregulates the atheroprotective hemoglobin receptor CD163 in human macrophages

RATIONALE: CXCL4 is a platelet-derived chemokine that promotes macrophage differentiation from monocytes. Deletion of the PF4 gene that encodes CXCL4 reduces atherosclerotic lesions in ApoE(-/-) mice. - OBJECTIVE: We sought to study effects of CXCL4 on macrophage differentiation with possible releva...

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Bibliographic Details
Main Authors: Gleißner, Christian A. (Author) , Shaked, Iftach (Author) , Erbel, Christian (Author) , Böckler, Dittmar (Author) , Katus, Hugo (Author) , Ley, Klaus (Author)
Format: Article (Journal)
Language:English
Published: 2010 January 8
In: Journal of banking and finance
Year: 2010, Volume: 106, Issue: 1, Pages: 203-211
ISSN:1872-6372
Online Access: Get full text
Author Notes:Christian A. Gleissner, Iftach Shaked, Christian Erbel, Dittmar Böckler, Hugo A. Katus, and Klaus Ley

MARC

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520 |a RATIONALE: CXCL4 is a platelet-derived chemokine that promotes macrophage differentiation from monocytes. Deletion of the PF4 gene that encodes CXCL4 reduces atherosclerotic lesions in ApoE(-/-) mice. - OBJECTIVE: We sought to study effects of CXCL4 on macrophage differentiation with possible relevance for atherogenesis. - METHODS AND RESULTS: Flow cytometry for expression of surface markers in macrophage colony-stimulating factor (M-CSF)- and CXCL4-induced macrophages demonstrated virtually complete absence of the hemoglobin scavenger receptor CD163 in CXCL4-induced macrophages. mRNA for CD163 was downregulated as early as 2 hours after CXCL4. CD163 protein reached a minimum after 3 days, which was not reversed by treatment of cells with M-CSF. The CXCL4 effect was entirely neutralized by heparin, which bound CXCL4 and prevented CXCL4 surface binding to monocytes. Pretreatment of cells with chlorate, which inhibits glycosaminoglycan synthesis, strongly inhibited CXCL4-dependent downregulation of CD163. Similar to recombinant CXCL4, releasate from human platelets also reduced CD163 expression. CXCL4-differentiated macrophages were unable to upregulate the atheroprotective enzyme heme oxygenase-1 at the RNA and protein level in response to hemoglobin-haptoglobin complexes. Immunofluorescence of human atherosclerotic plaques demonstrated presence of both CD68+CD163+ and CD68+CD163- macrophages. PF4 and CD163 gene expression within human atherosclerotic lesions were inversely correlated, supporting the in vivo relevance of CXCL4-induced downregulation of CD163. - CONCLUSIONS: CXCL4 may promote atherogenesis by suppressing CD163 in macrophages, which are then unable to upregulate the atheroprotective enzyme heme oxygenase-1 in response to hemoglobin. 
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650 4 |a Antigens, Differentiation, Myelomonocytic 
650 4 |a Apolipoproteins E 
650 4 |a Atherosclerosis 
650 4 |a Cell Differentiation 
650 4 |a Gene Expression Regulation 
650 4 |a Heme Oxygenase-1 
650 4 |a Hemoglobins 
650 4 |a Humans 
650 4 |a Macrophages 
650 4 |a Mice 
650 4 |a Mice, Knockout 
650 4 |a Monocytes 
650 4 |a Platelet Factor 4 
650 4 |a Receptors, Cell Surface 
650 4 |a Receptors, Scavenger 
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