Caveolin-1 regulates the anti-atherogenic properties of macrophages

Atherosclerosis is a complex disease initiated by the vascular accumulation of lipoproteins in the sub-endothelial space, followed by the infiltration of monocytes into the arterial intima. Caveolin-1 (Cav-1) plays an essential role in the regulation of cellular cholesterol metabolism and of various...

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Published in:	Cell and tissue research Vol. 358; no. 3; pp. 821 - 831
Main Authors:	Pavlides, Stephanos, Gutierrez-Pajares, Jorge L, Katiyar, Sanjay, Jasmin, Jean-François, Mercier, Isabelle, Walters, Rhonda, Pavlides, Christos, Pestell, Richard G, Lisanti, Michael P, Frank, Philippe G
Format:	Journal Article
Language:	English
Published:	Berlin/Heidelberg Springer-Verlag 01.12.2014 Springer Berlin Heidelberg Springer Springer Nature B.V Springer Verlag
Subjects:	Analysis Animals apoptosis Apoptosis - drug effects Atherosclerosis Atherosclerosis - blood Atherosclerosis - pathology Biochemistry Biochemistry, Molecular Biology Biomedical and Life Sciences Biomedicine Blood lipids bone marrow Bone Marrow Transplantation Cancer Cardiovascular disease Caveolin 1 - deficiency Caveolin 1 - metabolism Cell Behavior Cellular Biology Cholesterol cholesterol metabolism Cytokines - secretion Development and progression endothelial cells Food and Nutrition Human Genetics inflammation Inflammation - pathology Life Sciences Lipopolysaccharides - pharmacology Lipoproteins Lipoproteins - blood Macrophages Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - pathology Mice, Inbred C57BL Molecular biology Molecular Medicine monocytes Physiological aspects Proteomics Regular Article Rodents Signal transduction Subcellular Processes Up-Regulation - drug effects Lipoproteins Caveolae Mouse Caveolin Atherosclerosis Macrophage
ISSN:	0302-766X, 1432-0878, 1432-0878
Online Access:	Get full text
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Summary:	Atherosclerosis is a complex disease initiated by the vascular accumulation of lipoproteins in the sub-endothelial space, followed by the infiltration of monocytes into the arterial intima. Caveolin-1 (Cav-1) plays an essential role in the regulation of cellular cholesterol metabolism and of various signaling pathways. In order to study specifically the role of macrophage Cav-1 in atherosclerosis, we used Cav-1⁻/⁻Apoe⁻/⁻mice and transplanted them with bone marrow (BM) cells obtained from Cav-1⁺/⁺Apoe⁻/⁻or Cav-1⁻/⁻Apoe⁻/⁻mice and vice versa. We found that Cav-1⁺/⁺mice harboring Cav-1⁻/⁻BM-derived macrophages developed significantly larger lesions than Cav-1⁺/⁺mice harboring Cav-1⁺/⁺BM-derived macrophages. Cav-1⁻/⁻macrophages were more susceptible to apoptosis and more prone to induce inflammation. The present study provides clear evidence that the absence of Cav-1 in macrophage is pro-atherogenic, whereas its absence in endothelial cells protects against atherosclerotic lesion formation. These findings demonstrate the cell-specific role of Cav-1 during the development of this disease.
Bibliography:	http://dx.doi.org/10.1007/s00441-014-2008-4 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23
ISSN:	0302-766X 1432-0878 1432-0878
DOI:	10.1007/s00441-014-2008-4