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Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis

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Title: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis
Author: MacDonald, Marcia L. E.; van Eck, Miranda; Hildebrand, Reeni B.; Wong, Brian W. C.; Bissada, Nagat; Ruddle, Piers; Kontush, Anatol; Hussein, Hala; Pouladi, Mahmoud A.; Chapman, M. John; Fievet, Catherine; van Berkel, Theo J. C.; Staels, Bart; McManus, Bruce M.; Hayden, Michael R.
Subject Keywords Apolipoproteins;Atherosclerosis;Hyperlipoproteinemia;Inflammation;Lipoproteins
Issue Date: 2008-12-18
Publicly Available in cIRcle 2009-06-18
Publisher American Heart Association
Citation: Arteriosclerosis, Thrombosis, and Vascular Biology, 29(3), 341-347. http://atvb.ahajournals.org/cgi/content/full/29/3/341
Abstract: OBJECTIVE—Absence of stearoyl-CoA desaturase-1 (SCD1) in mice reduces plasma triglycerides and provides protection from obesity and insulin resistance, which would be predicted to be associated with reduced susceptibility to atherosclerosis. The aim of this study was to determine the effect of SCD1 deficiency on atherosclerosis. Methods and RESULTS—Despite an antiatherogenic metabolic profile, SCD1 deficiency increases atherosclerosis in hyperlipidemic low density lipoprotein receptor (LDLR)-deficient mice challenged with a western diet. Lesion area at the aortic root is significantly increased in males and females in two models of SCD1 deficiency. Inflammatory changes are evident in the skin of these mice, including increased intercellular adhesion molecule (ICAM)-1 and ulcerative dermatitis. Increases in ICAM-1 and interleukin-6 are also evident in plasma of SCD1-deficient mice. HDL particles demonstrate changes associated with inflammation, including, decreased plasma apoA-II and apoA-I and paraoxonase-1 and increased plasma serum amyloid A. Lipopolysaccharide-induced inflammatory response and cholesterol efflux are not altered in SCD1-deficient macrophages. In addition, when SCD1 deficiency is limited to bone-marrow derived cells, lesion size is not altered in LDLR-deficient mice. CONCLUSIONS—These studies reinforce the crucial role of chronic inflammation in promoting atherosclerosis, even in the presence of antiatherogenic biochemical and metabolic characteristics. [The original version of this article, along with updated information and services is located on the World Wide Web at: http://atvb.ahajournals.org/cgi/content/full/29/3/341] [UBC users: please click on the UBC eLink icon at the bottom of this record]
Affiliation: Child and Family Research Institute (CFRI)Medicine, Faculty ofMedical Genetics, Department ofMolecular Medicine and Therapeutics, Centre for
URI: http://hdl.handle.net/2429/9434
Peer Review Status: Reviewed
Scholarly Level: Faculty

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