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Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2002-12-3893. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-12-3893v1 101/12/4680    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 Christopherson, K. W. Articles by Broxmeyer, H. E. Search for Related Content PubMed PubMed Citation Articles by Christopherson, K. W., II Articles by Broxmeyer, H. E. Related Collections Hematopoiesis and Stem Cells Cell Adhesion and Motility Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 June 2003, Vol. 101, No. 12, pp. 4680-4686 CHEMOKINES Cell surface peptidase CD26/DPPIV mediates G-CSF mobilization of mouse progenitor cells Kent W. Christopherson, II, Scott Cooper, and Hal E. Broxmeyer From the Department of Microbiology/Immunology and the Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN; and the Walther Cancer Institute, Indianapolis, IN. CXC ligand 12 (CXCL12; also known as stromal cell–derived factor 1/SDF-1) chemoattracts hematopoietic stem and progenitor cells (HSCs/HPCs) and is thought to play a crucial role in the mobilization of HSCs/HPCs from the bone marrow. CD26 (dipeptidylpeptidase IV [DPPIV]) is a membrane-bound extracellular peptidase that cleaves dipeptides from the N-terminus of polypeptide chains. CD26 has the ability to cleave CXCL12 at its position-2 proline. We found by flow cytometry that CD26 is expressed on a subpopulation of normal Sca-1+c-kit+lin— hematopoietic cells isolated from mouse bone marrow, as well as Sca-1+c-kit—lin— cells, and that these cells possess CD26 peptidase activity. To test the functional role of CD26 in CXCL12-mediated normal HSC/HPC migration, chemotaxis assays were performed. The CD26 truncated CXCL12(3-68) showed an inability to induce the migration of sorted Sca-1+c-kit+lin— or Sca-1+c-kit—lin— mouse marrow cells compared with the normal CXCL12. In addition, CXCL12(3-68) acts as an antagonist, resulting in the reduction of migratory response to normal CXCL12. Treatment of Sca-1+c-kit+lin— mouse marrow cells, and myeloid progenitors within this population, or Sca-1+c-kit—lin— cells with a specific CD26 inhibitor, enhanced the migratory response of these cells to CXCL12. Finally, to test for potential in vivo relevance of these in vitro observations, mice were treated with CD26 inhibitors during granulocyte colony-stimulating factor (G-CSF)–induced mobilization. This treatment resulted in a reduction in the number of progenitor cells in the periphery as compared with the G-CSF regimen alone. This suggests that a mechanism of action of G-CSF mobilization involves CD26. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Prabhash, N. Khattry, A. Bakshi, R. Karandikar, A. Joshi, S. Kannan, P. S. R. K. Sastry, P. Parikh, and J. A. 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