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 |
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| Hlavní autoři: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
Berlin/Heidelberg
Springer-Verlag
01.12.2014
Springer Berlin Heidelberg Springer Springer Nature B.V Springer Verlag |
| Témata: | |
| ISSN: | 0302-766X, 1432-0878, 1432-0878 |
| On-line přístup: | Získat plný text |
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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. |
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| Bibliografie: | 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 |