
Pontus Dunér
Assistant researcher

Plasma fibronectin deficiency impedes atherosclerosis progression and fibrous cap formation
Author
Summary, in English
Atherosclerotic lesions are asymmetric focal thickenings of the intima of arteries that consist of lipids, various cell types and extracellular matrix (ECM). These lesions lead to vascular occlusion representing the most common cause of death in the Western world. The main cause of vascular occlusion is rupture of atheromatous lesions followed by thrombus formation. Fibronectin (FN) is one of the earliest ECM proteins deposited at atherosclerosis-prone sites and was suggested to promote atherosclerotic lesion formation. Here, we report that atherosclerosis-prone apolipoprotein E-null mice lacking hepatocyte-derived plasma FN (pFN) fed with a pro-atherogenic diet display dramatically reduced FN depositions at atherosclerosis-prone areas, which results in significantly smaller and fewer atherosclerotic plaques. However, the atherosclerotic lesions from pFN-deficient mice lacked vascular smooth muscle cells and failed to develop a fibrous cap. Thus, our results demonstrate that while FN worsens the course of atherosclerosis by increasing the atherogenic plaque area, it promotes the formation of the protective fibrous cap, which in humans prevents plaques rupture and vascular occlusion. See accompanying article http://dx.doi.org/10.1002/emmm.201200238
Department/s
- Cardiovascular Research - Immunity and Atherosclerosis
- EXODIAB: Excellence of Diabetes Research in Sweden
- EpiHealth: Epidemiology for Health
Publishing year
2012
Language
English
Pages
564-576
Publication/Series
EMBO Molecular Medicine
Volume
4
Issue
7
Document type
Journal article
Publisher
Wiley-Blackwell
Topic
- Cell and Molecular Biology
Keywords
- atherosclerosis
- fibronectin
- fibrous cap
- inflammation
- migration
Status
Published
Research group
- Cardiovascular Research - Immunity and Atherosclerosis
ISBN/ISSN/Other
- ISSN: 1757-4684