Please use this identifier to cite or link to this item:
Title: Plasma fibronectin deficiency impedes atherosclerosis progression and fibrous cap formation
Author: Rohwedder, Ina
Montañez, Eloi
Beckmann, Karsten
Bengtsson, Eva
Dunér, Pontus
Nilsson, Jan
Soehnlein, Oliver
Fässler, Reinhard
Keywords: Aterosclerosi
Issue Date: 1-Jul-2012
Publisher: EMBO Press
Abstract: 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.
Note: Reproducció del document publicat a:
It is part of: EMBO Molecular Medicine, 2012, vol. 4, num. 7, p. 564-576
Related resource:
ISSN: 1757-4676
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

Files in This Item:
File Description SizeFormat 
699841.pdf1.25 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.