SEARCH:   Advanced

Blood, 26 February 2009, Vol. 113, No. 9, pp. 1919-1928. Prepublished online as a Blood First Edition Paper on December 24, 2008; DOI 10.1182/blood-2008-06-159574. This Article Full Text Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2008-06-159574v1 113/9/1919    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 Praetor, A. Articles by Fong, S. Search for Related Content PubMed PubMed Citation Articles by Praetor, A. Articles by Fong, S. Related Collections Hematopoiesis and Stem Cells Phagocytes, Granulocytes, and Myelopoiesis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS AND STEM CELLS Genetic deletion of JAM-C reveals a role in myeloid progenitor generation Asja Praetor1, Jacqueline M. McBride1, Henry Chiu1, Linda Rangell2, Lorena Cabote2, Wyne P. Lee1, James Cupp1, Dimitry M. Danilenko2, and Sherman Fong1 Departments of 1 Immunology and 2 Pathology, Genentech, South San Francisco, CA Hematopoietic stem cells (HSCs) have the capacity to self-renew and continuously differentiate into all blood cell lineages throughout life. At each branching point during differentiation, interactions with the environment are key in the generation of daughter cells with distinct fates. Here, we examined the role of the cell adhesion molecule JAM-C, a protein known to mediate cellular polarity during spermatogenesis, in hematopoiesis. We show that murine JAM-C is highly expressed on HSCs in the bone marrow (BM). Expression correlates with self-renewal, the highest being on long-term repopulating HSCs, and decreases with differentiation, which is maintained longest among myeloid committed progenitors. Inclusion of JAM-C as a sole marker on lineage-negative BM cells yields HSC enrichments and long-term multilineage reconstitution when transferred to lethally irradiated mice. Analysis of Jam-C–deficient mice showed that two-thirds die within 48 hours after birth. In the surviving animals, loss of Jam-C leads to an increase in myeloid progenitors and granulocytes in the BM. Stem cells and myeloid cells from fetal liver are normal in number and homing to the BM. These results provide evidence that JAM-C defines HSCs in the BM and that JAM-C plays a role in controlling myeloid progenitor generation in the BM. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Scheiermann, B. Colom, P. Meda, N. S.A. Patel, M.-B. Voisin, A. Marrelli, A. Woodfin, C. Pitzalis, C. Thiemermann, M. Aurrand-Lions, et al. Junctional Adhesion Molecule-C Mediates Leukocyte Infiltration in Response to Ischemia Reperfusion Injury Arterioscler Thromb Vasc Biol, October 1, 2009; 29(10): 1509 - 1515. [Abstract] [Full Text] [PDF]

	Copyright © 2009 by American Society of Hematology         Online ISSN: 1528-0020