Protective role for properdin in progression of experimental murine atherosclerosis.

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 alternativ...

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Autores principales:	Tanja Steiner, Lorenza Francescut, Simon Byrne, Timothy Hughes, Archana Jayanthi, Irina Guschina, John Harwood, Katherine Cianflone, Cordula Stover, Sheila Francis
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/6e7e2dc8de124d9abcd1e4d12be77a54
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spelling	oai:doaj.org-article:6e7e2dc8de124d9abcd1e4d12be77a542021-11-18T08:26:13ZProtective role for properdin in progression of experimental murine atherosclerosis.1932-620310.1371/journal.pone.0092404https://doaj.org/article/6e7e2dc8de124d9abcd1e4d12be77a542014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24667818/?tool=EBIhttps://doaj.org/toc/1932-6203Genetic, 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(-/-) 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(-/-) Properdin(KO) (LDLR(-/-)P(KO)) and LDLR-/-PWT mice. Lipids, lymphocytes and monocytes were similar among genotypes, genders and diets. Complement C3, but not C3adesarg, levels were enhanced in LDLR(-/-)P(KO) mice regardless of diet type or gender. Non-esterified fatty acids (NEFA) were decreased in male LDLR(-/-)P(KO) fed a HFD compared with controls. All mice showed significant atherosclerotic burden in aortae and at aortic roots but male LDLR(-/-) 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(-/-)mice when fed a HFD. We conclude that properdin plays an unexpectedly beneficial role in the development and progression of early atherosclerotic lesions.Tanja SteinerLorenza FrancescutSimon ByrneTimothy HughesArchana JayanthiIrina GuschinaJohn HarwoodKatherine CianfloneCordula StoverSheila FrancisPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 3, p e92404 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tanja Steiner Lorenza Francescut Simon Byrne Timothy Hughes Archana Jayanthi Irina Guschina John Harwood Katherine Cianflone Cordula Stover Sheila Francis Protective role for properdin in progression of experimental murine atherosclerosis.
description	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(-/-) 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(-/-) Properdin(KO) (LDLR(-/-)P(KO)) and LDLR-/-PWT mice. Lipids, lymphocytes and monocytes were similar among genotypes, genders and diets. Complement C3, but not C3adesarg, levels were enhanced in LDLR(-/-)P(KO) mice regardless of diet type or gender. Non-esterified fatty acids (NEFA) were decreased in male LDLR(-/-)P(KO) fed a HFD compared with controls. All mice showed significant atherosclerotic burden in aortae and at aortic roots but male LDLR(-/-) 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(-/-)mice when fed a HFD. We conclude that properdin plays an unexpectedly beneficial role in the development and progression of early atherosclerotic lesions.
format	article
author	Tanja Steiner Lorenza Francescut Simon Byrne Timothy Hughes Archana Jayanthi Irina Guschina John Harwood Katherine Cianflone Cordula Stover Sheila Francis
author_facet	Tanja Steiner Lorenza Francescut Simon Byrne Timothy Hughes Archana Jayanthi Irina Guschina John Harwood Katherine Cianflone Cordula Stover Sheila Francis
author_sort	Tanja Steiner
title	Protective role for properdin in progression of experimental murine atherosclerosis.
title_short	Protective role for properdin in progression of experimental murine atherosclerosis.
title_full	Protective role for properdin in progression of experimental murine atherosclerosis.
title_fullStr	Protective role for properdin in progression of experimental murine atherosclerosis.
title_full_unstemmed	Protective role for properdin in progression of experimental murine atherosclerosis.
title_sort	protective role for properdin in progression of experimental murine atherosclerosis.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/6e7e2dc8de124d9abcd1e4d12be77a54
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Protective role for properdin in progression of experimental murine atherosclerosis.

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