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CXCL5 limits macrophage foam cell formation in atherosclerosis.

The Journal of clinical investigation

Up-Regulation, ATP-Binding Cassette Transporters, genetics, metabolism, Animals, Aorta, Apolipoproteins E, deficiency, Atherosclerosis, blood, immunology, Chemokine CXCL5, physiology, Cholesterol, secretion, Endothelial Cells, Foam Cells, Macrophage Activation, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Plaque, Atherosclerotic, pathology, RNA, Messenger, Receptors, Interleukin-8B, Transcriptional Activation, ATP Binding Cassette Transporter 1

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      Abstract

      The ELR(+)-CXCL chemokines have been described typically as potent chemoattractants and activators of neutrophils during the acute phase of inflammation. Their role in atherosclerosis, a chronic inflammatory vascular disease, has been largely unexplored. Using a mouse model of atherosclerosis, we found that CXCL5 expression was upregulated during disease progression, both locally and systemically, but was not associated with neutrophil infiltration. Unexpectedly, inhibition of CXCL5 was not beneficial but rather induced a significant macrophage foam cell accumulation in murine atherosclerotic plaques. Additionally, we demonstrated that CXCL5 modulated macrophage activation, increased expression of the cholesterol efflux regulatory protein ABCA1, and enhanced cholesterol efflux activity in macrophages. These findings reveal a protective role for CXCL5, in the context of atherosclerosis, centered on the regulation of macrophage foam cell formation.

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      Journal
      10.1172/JCI66580
      23376791
      3582141

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