| First Author | Sauter M | Year | 2022 |
| Journal | iScience | Volume | 25 |
| Issue | 1 | Pages | 103677 |
| PubMed ID | 35036868 | Mgi Jnum | J:321395 |
| Mgi Id | MGI:6856474 | Doi | 10.1016/j.isci.2021.103677 |
| Citation | Sauter M, et al. (2022) Apolipoprotein E derived from CD11c(+) cells ameliorates atherosclerosis. iScience 25(1):103677 |
| abstractText | Atherosclerosis is studied in models with dysfunctional lipid homeostasis-predominantly the ApoE(-/-) mouse. The role of antigen-presenting cells (APCs) for lipid homeostasis is not clear. Using a LacZ reporter mouse, we showed that CD11c(+) cells were enriched in aortae of ApoE(-/-) mice. Systemic long-term depletion of CD11c(+) cells in ApoE(-/-) mice resulted in significantly increased plaque formation associated with reduced serum ApoE levels. In CD11c(cre+)ApoE(fl/fl) and Albumin(cre+)ApoE(fl/fl) mice, we could show that approximately 70% of ApoE is liver-derived and approximately 25% originates from CD11c(+) cells associated with significantly increased atherosclerotic plaque burden in both strains. Exposure to acLDL promoted cholesterol efflux from CD11c(+) cells and cell-specific deletion of ApoE resulted in increased inflammation reflected by increased IL-1beta serum levels. Our results determined for the first time the level of ApoE originating from CD11c(+) cells and demonstrated that CD11c(+) cells ameliorate atherosclerosis by the secretion of ApoE. |
