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Blood, 1 July 2004, Vol. 104, No. 1, pp. 11-18. Prepublished online as a Blood First Edition Paper on February 19, 2004; DOI 10.1182/blood-2003-09-3363. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-09-3363v1 104/1/11    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tan, M. H. Articles by George, E. L. Search for Related Content PubMed PubMed Citation Articles by Tan, M. H. Articles by George, E. L. Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Plenary Papers Cell Adhesion and Motility Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLENARY PAPERS Deletion of the alternatively spliced fibronectin EIIIA domain in mice reduces atherosclerosis Michelle H. Tan, Zhengwu Sun, Sarah L. Opitz, Tracy E. Schmidt, John H. Peters, and Elizabeth L. George From the Vascular Research Division, Department of Pathology, Brigham and Women's Hospital, Boston, MA; the Department of Pathology, Harvard Medical School, Boston, MA; the Department of Medicine, Veterans Administration (VA) Northern California Health Care System, Sacramento VA Medical Center, Mather, CA; and the Department of Internal Medicine, University of California School of Medicine, Davis. The alternatively spliced and highly conserved EIIIA domain of fibronectin (FN) is included in most FN of the extracellular matrix in embryos. In adults, both extracellular matrix and plasma FN essentially lack EIIIA. In diverse inflammatory situations however, EIIIA is specifically included by regulated RNA splicing. In atherosclerotic lesions, FN, including the EIIIA domain (EIIIA-FN), is abundant, whereas FN in the flanking vessel wall lacks EIIIA. Lesional EIIIA-FN is localized with endothelial cells and macrophage foam cells. To directly test the function of EIIIA-FN, we generated EIIIA-null (EIIIA–/–) mice that lack the EIIIA exon and crossed them with apolipoprotein E (ApoE)–null (ApoE–/–) mice that develop arterial wall lesions. Compared with ApoE–/– controls, EIIIA–/–ApoE–/– mice had significantly smaller lesions throughout the aortic tree. EIIIA-FN was increased in ApoE–/– plasma, and total plasma cholesterol was reduced in EIIIA–/–ApoE–/– mice, specifically in large lipoprotein particles, suggesting a functional role for plasma EIIIA-FN. To assess a role for macrophage EIIIA-FN in the vessel wall, we conducted in vitro foam cell assays. EIIIA–/–ApoE–/– macrophages accumulated significantly less intracellular lipid than control ApoE–/– cells. These results provide genetic evidence that suggests roles for EIIIA-FN in plasma lipoprotein metabolism and in foam cell formation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Atherogenic role of the type EIIIA fibronectin domain Vicente Andrés Blood 2004 104: 3-4. [Full Text] [PDF] This article has been cited by other articles: D. F. Mosher Adding Complexity to Fibronectin-Platelet Interactions Arterioscler. Thromb. Vasc. Biol., February 1, 2008; 28(2): 203 - 204. [Full Text] [PDF] A. V. Shinde, C. Bystroff, C. Wang, M. G. Vogelezang, P. A. Vincent, R. O. Hynes, and L. Van De Water Identification of the Peptide Sequences within the EIIIA (EDA) Segment of Fibronectin That Mediate Integrin {alpha}9{beta}1-dependent Cellular Activities J. Biol. Chem., February 1, 2008; 283(5): 2858 - 2870. [Abstract] [Full Text] [PDF] A. K. Chauhan, J. Kisucka, M. R. Cozzi, M. T. Walsh, F. A. Moretti, M. Battiston, M. Mazzucato, L. De Marco, F. E. Baralle, D. D. Wagner, et al. Prothrombotic Effects of Fibronectin Isoforms Containing the EDA Domain Arterioscler. Thromb. Vasc. Biol., February 1, 2008; 28(2): 296 - 301. [Abstract] [Full Text] [PDF] H.-S. Li-Korotky, P. A. Hebda, C.-Y. Lo, and J. E. Dohar Age-Dependent Differential Expression of Fibronectin Variants in Skin and Airway Mucosal Wounds Arch Otolaryngol Head Neck Surg, September 1, 2007; 133(9): 919 - 924. [Abstract] [Full Text] [PDF] T. Moroy and F. 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Arditi TLR Signaling: An Emerging Bridge from Innate Immunity to Atherogenesis J. Immunol., November 15, 2004; 173(10): 5901 - 5907. [Abstract] [Full Text] [PDF] S. Astrof, D. Crowley, E. L. George, T. Fukuda, K. Sekiguchi, D. Hanahan, and R. O. Hynes Direct Test of Potential Roles of EIIIA and EIIIB Alternatively Spliced Segments of Fibronectin in Physiological and Tumor Angiogenesis Mol. Cell. Biol., October 1, 2004; 24(19): 8662 - 8670. [Abstract] [Full Text] [PDF]

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