Matches in UGent Biblio for { <https://biblio.ugent.be/publication/3049571#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B239340.
- aggregation creator B239341.
- aggregation creator B239342.
- aggregation creator B239343.
- aggregation creator person.
- aggregation date "2012".
- aggregation format "application/pdf".
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- aggregation isPartOf urn:issn:0009-7322.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Conditional targeting of tumor necrosis factor receptor-associated factor 6 reveals opposing functions of toll-like receptor signaling in endothelial and myeloid cells in a mouse model of atherosclerosis".
- aggregation abstract "Background : Previous studies implicated Toll-like receptor signaling as a critical pathogenic pathway in atherosclerosis, but the cell-specific mechanisms by which Toll-like receptors act to control atherosclerotic plaque development remain poorly understood. Methods and Results : To study the cell-specific role of tumor necrosis factor receptor-associated factor 6 (TRAF6) in atherosclerosis, we generated ApoE(-/-) mice with endothelial cell-or myeloid cell-specific TRAF6 deficiency using Cre/LoxP-mediated gene targeting. Endothelial TRAF6 deficiency reduced atherosclerosis in female ApoE(-/-) mice by inhibiting nuclear factor-kappa B-dependent proinflammatory gene expression and monocyte adhesion to endothelial cells. In contrast, myeloid cell-specific TRAF6 deficiency caused exacerbated atherosclerosis, with larger plaques containing more necrotic areas in both male and female ApoE(-/-) mice. TRAF6-deficient macrophages showed impaired expression of the antiinflammatory and atheroprotective cytokine interleukin-10, elevated endoplasmic reticulum stress, increased sensitivity to oxidized low-density lipoprotein-induced apoptosis, and reduced capacity to clear apoptotic cells. Thus, the reduced antiinflammatory properties, coupled with increased sensitivity to apoptosis and impaired efferocytosis capacity of TRAF6-deficient macrophages, result in exacerbated atherosclerosis development in TRAF6(MYKO)/ApoE(-/-) mice. Conclusion : Toll-like receptor-mediated TRAF6 signaling acts in endothelial cells to promote atherosclerosis but displays atheroprotective, antiinflammatory and prosurvival functions in myeloid cells.".
- aggregation authorList BK511114.
- aggregation endPage "1751".
- aggregation issue "14".
- aggregation startPage "1739".
- aggregation volume "126".
- aggregation aggregates 4381337.
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