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Title: Protective role for properdin in progression of experimental murine atherosclerosis.
Authors: Steiner, T.
Francescut, Lorenza
Byrne, Simon
Hughes, T.
Jayanthi, A.
Guschina, I.
Harwood, J.
Cianflone, K.
Stover, Cordula
Francis, S.
First Published: 25-Mar-2014
Publisher: Public Library of Science
Citation: PLoS One, 2014, 9 (3), e92404
Abstract: Genetic, dietary and immune factors contribute to the pathogenesis of atherosclerosis in humans and mice. Complement activation is an integral part of the innate immune defence but also shapes cellular responses and influences directly triglyceride synthesis. Deficiency of Factor B of the alternative pathway (AP) of complement is beneficial in LDLR[superscript: -/-] mice fed a high fat diet. The serum glycoprotein properdin is a key positive regulator of the AP but has not been studied in experimental atherosclerosis. Atherosclerosis was assessed after feeding low fat (LFD) or high fat (HFD) Western type diets to newly generated LDLR[superscript: -/-] Properdin[superscript: KO] (LDLR[superscript: -/-]P[superscript: KO]) and LDLR[superscript: -/-PWT] mice. Lipids, lymphocytes and monocytes were similar among genotypes, genders and diets. Complement C3, but not C3[subscript: adesarg], levels were enhanced in LDLR[superscript: -/-]P[superscript: KO] mice regardless of diet type or gender. Non-esterified fatty acids (NEFA) were decreased in male LDLR[superscript: -/-]P[superscript: KO] fed a HFD compared with controls. All mice showed significant atherosclerotic burden in aortae and at aortic roots but male LDLR[superscript: -/-] mice fed a LFD were affected to the greatest extent by the absence of properdin. The protective effect of properdin expression was overwhelmed in both genders of LDLR[superscript: -/-]mice when fed a HFD. We conclude that properdin plays an unexpectedly beneficial role in the development and progression of early atherosclerotic lesions.
DOI Link: 10.1371/journal.pone.0092404
eISSN: 1932-6203
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2014 Steiner et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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