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dc.contributor.authorPavlides, Stephanos
dc.contributor.authorGutierrez-Pajares, J
dc.contributor.authorKatiyar, S
dc.contributor.authorJasmin, J
dc.contributor.authorMercier, I
dc.contributor.authorWalters, R
dc.contributor.authorPavlides, C
dc.contributor.authorPestell, R
dc.contributor.authorLisanti, Michael P
dc.contributor.authorFrank, P
dc.date.accessioned2014-11-10T09:53:47Z
dc.date.available2014-11-10T09:53:47Z
dc.date.issued2014-10-17
dc.identifier.citationCaveolin-1 regulates the anti-atherogenic properties of macrophages. 2014: Cell Tissue Resen
dc.identifier.issn1432-0878
dc.identifier.pmid25322709
dc.identifier.doi10.1007/s00441-014-2008-4
dc.identifier.urihttp://hdl.handle.net/10541/333862
dc.description.abstractAtherosclerosis 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.
dc.languageENG
dc.language.isoenen
dc.rightsArchived with thanks to Cell and tissue researchen
dc.titleCaveolin-1 regulates the anti-atherogenic properties of macrophages.en
dc.typeArticleen
dc.contributor.departmentManchester Breast Centre & Breakthrough Breast Cancer Research Unit, Paterson Institute for Cancer Research, School of Cancer, Enabling Sciences and Technology, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.en
dc.identifier.journalCell and Tissue Researchen
html.description.abstractAtherosclerosis 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.


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