SEARCH:   Advanced

Blood, 15 January 2006, Vol. 107, No. 2, pp. 796-805. Prepublished online as a Blood First Edition Paper on September 29, 2005; DOI 10.1182/blood-2005-05-1902. This Article Full Text (PDF) All Versions of this Article: 2005-05-1902v1 107/2/796    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 Cui, W. Articles by Vignery, A. Search for Related Content PubMed PubMed Citation Articles by Cui, W. Articles by Vignery, A. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 13, 2005 Accepted September 8, 2005 The intracellular domain of CD44 promotes the fusion of macrophages via NF-B Weiguo Cui, Juan Zhang Ke, Qing Zhang, Hua-Zhu Ke, Cecile Chalouni, and Agnes Vignery* Department of Orthopaedics and Rehabilitation, Yale School of Medicine, New Haven, CT, USA Pfizer Global Research and Development, Groton, CT, USA Department of Cell Biology, Yale School of Medicine, New Haven, CT, USA * Corresponding author; email: agnes.vignery{at}yale.edu. Macrophages seed all tissues in which they have the ability, in specific and rare instances, to fuse with themselves and to differentiate into osteoclasts in bone, or into giant cells in chronic inflammatory reactions. Although these cells play a central role in osteoporosis and in foreign body rejection, respectively, the molecular mechanism used by macrophages to fuse remains poorly understood. Macrophages might also fuse with somatic and tumor cells to promote tissue repair and metastasis, respectively. We reported that CD44 expression is highly, but transiently induced in macrophages at the onset of fusion in which it plays a role. We report now that the intracellular domain of CD44 (CD44ICD) is cleaved in macrophages undergoing fusion and that presenilin inhibitors prevent the release of CD44ICD and fusion. We also show that CD44ICD promotes the fusion of tissue macrophages and bone marrow-derived macrophages. Finally, we report that CD44ICD is localized in the nucleus of macrophages in which it promotes the activation of NF-B. These observations open avenues to study the role of CD44ICD in blood cells and tumors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B. K. McMichael, R. B. Wysolmerski, and B. S. Lee Regulated Proteolysis of Nonmuscle Myosin IIA Stimulates Osteoclast Fusion J. Biol. Chem., May 1, 2009; 284(18): 12266 - 12275. [Abstract] [Full Text] [PDF] A. M. Miller, M. J. Nolan, J. Choi, T. Koga, X. Shen, B. Y. J. T. Yue, and P. A. Knepper Lactate Treatment Causes NF-{kappa}B Activation and CD44 Shedding in Cultured Trabecular Meshwork Cells Invest. Ophthalmol. Vis. Sci., April 1, 2007; 48(4): 1615 - 1621. [Abstract] [Full Text] [PDF]

	Copyright © 2005 by American Society of Hematology         Online ISSN: 1528-0020