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Blood, 1 December 2004, Vol. 104, No. 12, pp. 3472-3482. Prepublished online as a Blood First Edition Paper on July 29, 2004; DOI 10.1182/blood-2003-12-4423. This Article Full Text (PDF) All Versions of this Article: 2003-12-4423v1 104/12/3472    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 De Falco, E. Articles by Pesce, M. Search for Related Content PubMed PubMed Citation Articles by De Falco, E. Articles by Pesce, M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 30, 2003 Accepted July 23, 2004 SDF-1 involvement in endothelial phenotype and ischemia-induced recruitment of bone marrow progenitor cells Elena De Falco, Daniele Porcelli, Anna Rita Torella, Stefania Straino, Maria Grazia Iachininoto, Alessia Orlandi, Silvia Truffa, Paolo Biglioli, Monica Napolitano, Maurizio C Capogrossi, and Maurizio Pesce* Laboratorio di Patologia Vascolare, Istituto Dermopatico dell' Immacolata, IDI-IRCCS, Rome, Italy Laboratorio di Biologia Vasolare e Terapia Genica, Centro Cardiologico Monzino, IRCCS, Milan, Italy * Corresponding author; email: m.pesce{at}idi.it. Chemokine SDF-1 is involved in trafficking of hematopoietic stem cells (HSCs) from the bone marrow (BM) to peripheral blood (PB) and has been found to enhance post-ischemia angiogenesis. This study was aimed at investigating whether SDF-1 plays a role in differentiation of BM-derived c-kit+ stem cells into endothelial progenitor cells (EPCs) and in ischemia-induced trafficking of stem cells from PB to ischemic tissues. We found that SDF-1 enhanced EPC number by promoting a2, a4 and a5 integrin-mediated adhesion to fibronectin and collagen I. EPC differentiation was reduced in mitogen-stimulated c-kit+ cells, while cytokine withdrawal or the overexpression of the cyclin-CDK inhibitor p16INK4 restored such differentiation suggesting a link between control of cell cycle and EPC differentiation. We also analyzed the time course of SDF-1 expression in a mouse model of hind limb ischemia. Shortly after femoral artery dissection, plasma SDF-1 levels were upregulated, while SDF-1 expression in the bone marrow was downregulated in a timely fashion with the increase in the percentage of PB progenitor cells. An increase in ischemic tissue expression of SDF-1 at RNA and protein level were also observed. Finally, using an in vivo assay such as injection of matrigel plugs, we found that SDF-1 improves formation of tubule-like structures by co-injected c-kit+ cells. Our findings unravel a function for SDF-1 in increase of EPC number and formation of vascular structures by bone marrow progenitor cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Zisa, A. Shabbir, M. Mastri, G. Suzuki, and T. Lee Intramuscular VEGF repairs the failing heart: role of host-derived growth factors and mobilization of progenitor cells Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2009; 297(5): R1503 - R1515. [Abstract] [Full Text] [PDF] Y. Shaked, T. Tang, J. Woloszynek, L. G. Daenen, S. Man, P. Xu, S.-R. Cai, J. M. Arbeit, E. E. Voest, D. J. Chaplin, et al. 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