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Vimentin deficiency in macrophages induces increased oxidative stress and vascular inflammation but attenuates atherosclerosis in mice

Journal article
Authors Liliana Håversen
J. P. Sundelin
A. Mardinoglu
Mikael Rutberg
Marcus Ståhlman
Ulrika Wilhelmsson
Lillemor Mattsson Hultén
Milos Pekny
Per Fogelstrand
J. F. Bentzon
Malin Levin
Jan Borén
Published in Scientific Reports
Volume 8
ISSN 2045-2322
Publication year 2018
Published at Wallenberg Laboratory
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Keywords low-density-lipoprotein, scavenger receptor, intermediate-filaments, lesion development, cd36, retention, activation, expression, identification, cholesterol, Science & Technology - Other Topics, lch j, 1957, journal of biological chemistry, v226, p497
Subject categories Cell biology


The aim was to clarify the role of vimentin, an intermediate filament protein abundantly expressed in activated macrophages and foam cells, in macrophages during atherogenesis. Global gene expression, lipid uptake, ROS, and inflammation were analyzed in bone-marrow derived macrophages from vimentin-deficient (Vim(-/-)) and wild-type (Vim(-/-)) mice. Atherosclerosis was induced in Ldlr(-/-) mice transplanted with a PCSK9 gain-of-function virus. The mice were fed an atherogenic diet for 12-15 weeks. We observed impaired uptake of native LDL but increased uptake of oxLDL in Vim(-/-) macrophages. FACS analysis revealed increased surface expression of the scavenger receptor CD36 on Vim(-/-) macrophages. Vim(-/-) macrophages also displayed increased markers of oxidative stress, activity of the transcription factor NF-kappa B, secretion of proinflammatory cytokines and GLUT1-mediated glucose uptake. Vim(-/- )mice displayed decreased atherogenesis despite increased vascular inflammation and increased CD36 expression on macrophages in two mouse models of atherosclerosis. We demonstrate that vimentin has a strong suppressive effect on oxidative stress and that Vim(-/-) mice display increased vascular inflammation with increased CD36 expression on macrophages despite decreased subendothelial lipid accumulation. Thus, vimentin has a key role in regulating inflammation in macrophages during atherogenesis.

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