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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Vydáno v:Cell and tissue research Ročník 358; číslo 3; s. 821 - 831
Hlavní autoři: 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
Médium: Journal Article
Jazyk:angličtina
Vydáno: Berlin/Heidelberg Springer-Verlag 01.12.2014
Springer Berlin Heidelberg
Springer
Springer Nature B.V
Springer Verlag
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ISSN:0302-766X, 1432-0878, 1432-0878
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Shrnutí: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.
Bibliografie:http://dx.doi.org/10.1007/s00441-014-2008-4
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ISSN:0302-766X
1432-0878
1432-0878
DOI:10.1007/s00441-014-2008-4