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Blood, 15 January 2004, Vol. 103, No. 2, pp. 710-716. Prepublished online as a Blood First Edition Paper on August 28, 2003; DOI 10.1182/blood-2003-02-0492. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-02-0492v1 103/2/710    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 Wandersee, N. J. Articles by Hillery, C. A. Search for Related Content PubMed PubMed Citation Articles by Wandersee, N. J. Articles by Hillery, C. A. Related Collections Cell Adhesion and Motility Hemostasis, Thrombosis, and Vascular Biology Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis Nancy J. Wandersee, Scott C. Olson, Sandra L. Holzhauer, Raymond G. Hoffmann, Jane E. Barker, and Cheryl A. Hillery From The Jackson Laboratory, Bar Harbor, ME; Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, WI; and Departments of Pediatrics and Biostatistics, Medical College of Wisconsin, Milwaukee, WI. Mice with disruptions of the red blood cell (RBC) cytoskeleton provide severe hemolytic anemia models in which to study multiorgan thrombosis and infarction. The incidence of cerebral infarction ranges from 70% to 100% in mice with -spectrin deficiency. To determine whether mutant RBCs abnormally bind adhesive vascular components, we measured adhesion of mouse and human RBCs to immobilized human thrombospondin (TSP) and laminin (LM) under controlled flow conditions. Mutant RBCs had at least 10-fold higher adhesion to TSP compared with normal RBCs (P < .006). Mutant relative to unaffected RBC adhesion to LM was significantly (P < .01) increased as well. Treatment of RBCs with the anionic polysaccharide dextran sulfate inhibited mutant RBC adhesion to TSP (P < .001). Treatment of RBCs with antibodies to CD47 or the CD47-binding TSP peptide 4N1K did not inhibit TSP adhesion of RBCs. Previously, we have shown that infarcts in -spectrin–deficient sph/sph mice become histologically evident beginning at 6 weeks of age. TSP adhesion of RBCs from 3- to 4- and 6- to 8-week-old sph/sph mice was significantly higher than RBCs from adult mice (> 12 weeks old; P < .005). While the mechanism of infarction in these mice is unknown, we speculate that changes in RBC adhesive characteristics contribute to this pathology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Rahuel, A. Filipe, L. Ritie, W. El Nemer, N. Patey-Mariaud, D. Eladari, J.-P. Cartron, P. Simon-Assmann, C. Le Van Kim, and Y. Colin Genetic inactivation of the laminin {alpha}5 chain receptor Lu/BCAM leads to kidney and intestinal abnormalities in the mouse Am J Physiol Renal Physiol, February 1, 2008; 294(2): F393 - F406. [Abstract] [Full Text] [PDF] N. S. Gov and S. A. Safran Red Blood Cell Membrane Fluctuations and Shape Controlled by ATP-Induced Cytoskeletal Defects Biophys. J., March 1, 2005; 88(3): 1859 - 1874. [Abstract] [Full Text] [PDF]

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