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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004376naa a2200697 4500
001oai:gup.ub.gu.se/206766
003SwePub
008240528s2014 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:129957308
024a https://gup.ub.gu.se/publication/2067662 URI
024a https://doi.org/10.1093/eurheartj/eht5322 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1299573082 URI
040 a (SwePub)gud (SwePub)ki
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Akhmedov, A.4 aut
2451 0a Endothelial overexpression of LOX-1 increases plaque formation and promotes atherosclerosis in vivo
264 c 2014-01-12
264 1b Oxford University Press (OUP),c 2014
520 a Aims Lectin-like oxLDL receptor-1 (LOX-1) mediates the uptake of oxidized low-density lipoprotein (oxLDL) in endothelial cells and macrophages. However, the different atherogenic potential of LOX-1-mediated endothelial and macrophage oxLDL uptake remains unclear. The present study was designed to investigate the in vivo role of endothelial LOX-1 in atherogenesis. Methods and results Endothelial-specific LOX-1 transgenic mice were generated using the Tie2 promoter (LOX-1TG). Oxidized low-density lipoprotein uptake was enhanced in cultured endothelial cells, but not in macrophages of LOX-1TG mice. Six-week-old male LOX-1TG and wild-type (WT) mice were fed a high-cholesterol diet (HCD) for 30 weeks. Increased reactive oxygen species production, impaired endothelial nitric oxide synthase activity and endothelial dysfunction were observed in LOX-1TG mice as compared with WT littermates. LOX-1 overexpression led to p38 phosphorylation, increased nuclear factor kappa B activity and subsequent up-regulation of vascular cell adhesion molecule-1, thereby favouring macrophage accumulation and aortic fatty streaks. Consistently, HCD-fed double-mutant LOX-1TG/ApoE(-/-) displayed oxidative stress and vascular inflammation with higher aortic plaques than ApoE(-/-) controls. Finally, bone marrow transplantation experiments showed that endothelial LOX-1 was sufficient for atherosclerosis development in vivo. Conclusions Endothelial-specific LOX-1 overexpression enhanced aortic oxLDL levels, thereby favouring endothelial dysfunction, vascular inflammation and plaque formation. Thus, LOX-1 may serve as a novel therapeutic target for atherosclerosis.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
653 a Endothelium
653 a Vascular inflammation
653 a Atherosclerosis
653 a LOW-DENSITY-LIPOPROTEIN
653 a ADHESION MOLECULE EXPRESSION
653 a LECTIN-LIKE
653 a OX-LDL
653 a MONOCYTE ADHESION
653 a KNOCKOUT MICE
653 a CELLS
653 a RECEPTOR-1
653 a ATHEROGENESIS
653 a APOPTOSIS
700a Rozenberg, I.4 aut
700a Paneni, F.u Karolinska Institutet4 aut
700a Camici, G. G.4 aut
700a Shi, Y.4 aut
700a Doerries, C.4 aut
700a Sledzinska, A.4 aut
700a Mocharla, P.4 aut
700a Breitenstein, A.4 aut
700a Lohmann, C.4 aut
700a Stein, S.4 aut
700a von Lukowicz, T.4 aut
700a Kurrer, M. O.4 aut
700a Borén, Jan,d 1963u Gothenburg University,Göteborgs universitet,Center for Cardiovascular and Metabolic Research (CMR)4 aut0 (Swepub:gu)xborej
700a Becher, B.4 aut
700a Tanner, F. C.4 aut
700a Landmesser, U.4 aut
700a Matter, C. M.4 aut
700a Luscher, T. F.4 aut
710a Karolinska Institutetb Center for Cardiovascular and Metabolic Research (CMR)4 org
773t European Heart Journald : Oxford University Press (OUP)g 35:40, s. 2839-2848q 35:40<2839-2848x 0195-668Xx 1522-9645
856u https://academic.oup.com/eurheartj/article-pdf/35/40/2839/17354717/eht532.pdf
8564 8u https://gup.ub.gu.se/publication/206766
8564 8u https://doi.org/10.1093/eurheartj/eht532
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:129957308

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