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Arachidonate 15-Lipoxygenase Type B Knockdown Leads to Reduced Lipid Accumulation and Inflammation in Atherosclerosis

Journal article
Authors Lisa U. Magnusson
Annika Lundqvist
Merja Nurkkala Karlsson
Kristina Skålen
Max Levin
Olov Wiklund
Jan Borén
Lillemor Mattsson Hultén
Published in Plos One
Volume 7
Issue 8
Pages e43142
ISSN 1932-6203
Publication year 2012
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages e43142
Language en
Links dx.doi.org/10.1371/journal.pone.004...
Keywords double-edged-sword, oxidative modification, deficient mice, expression, ldl, 8s-lipoxygenase, identification, interleukin-2, angiogenesis, macrophages
Subject categories Cell and Molecular Biology

Abstract

Inflammation in the vascular wall is important for development of atherosclerosis. We have shown previously that arachidonate 15-lipoxygenase type B (ALOX15B) is more highly expressed in human atherosclerotic lesions than in healthy arteries. This enzyme oxidizes fatty acids to substances that promote local inflammation and is expressed in lipid-loaded macrophages (foam cells) present in the atherosclerotic lesions. Here, we investigated the role of ALOX15B in foam cell formation in human primary macrophages and found that silencing of human ALOX15B decreased cellular lipid accumulation as well as proinflammatory cytokine secretion from macrophages. To investigate the role of ALOX15B in promoting the development of atherosclerosis in vivo, we used lentiviral shRNA silencing and bone marrow transplantation to knockdown mouse Alox15b gene expression in LDL-receptor-deficient (Ldlr(-/-)) mice. Knockdown of mouse Alox15b in vivo decreased plaque lipid content and markers of inflammation. In summary, we have shown that ALOX15B influences progression of atherosclerosis, indicating that this enzyme has an active proatherogenic role.

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