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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 (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 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 Related Article in Blood Online Social Bookmarking                   What's this? Submitted September 30, 2003 Accepted December 19, 2003 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* Pathology, Vascular Research Divsion, Brigham and Women's Hospital, Boston, MA, USA; Pathology, Harvard Medical School, Boston, MA, USA Pathology, Vascular Research Divsion, Brigham and Women's Hospital, Boston, MA, USA Medicine, University of California School of Medicine, Davis, CA, USA Pathology, Vascular Research Divsion, Brigham and Women's Hospital, Boston, MA, USA; Medicine, University of California School of Medicine, Davis, CA, USA * Corresponding author; email: egeorge{at}rics.bwh.harvard.edu. 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, while 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 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: S. M. Edwards-Bennett, L. M. Jacks, C. H. Moskowitz, E. J. Wu, Z. Zhang, A. Noy, C. S. Portlock, D. J. Straus, A. D. Zelenetz, and J. Yahalom Stanford V program for locally extensive and advanced Hodgkin lymphoma: the Memorial Sloan-Kettering Cancer Center experience Ann. Onc., September 16, 2009; (2009) mdp337v1. [Abstract] [Full Text] [PDF] B. S. Fleenor and D. K. 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