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Blood, 1 March 2005, Vol. 105, No. 5, pp. 1916-1922. Prepublished online as a Blood First Edition Paper on November 16, 2004; DOI 10.1182/blood-2004-09-3415. This Article Full Text Full Text (PDF) Supplemental Video All Versions of this Article: 2004-09-3415v1 105/5/1916    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 Guthrie, S. M. Articles by Scott, E. W. Search for Related Content PubMed PubMed Citation Articles by Guthrie, S. M. Articles by Scott, E. W. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS The nitric oxide pathway modulates hemangioblast activity of adult hematopoietic stem cells Steven M. Guthrie, Lisa M. Curtis, Robert N. Mames, Gregory G. Simon, Maria B. Grant, and Edward W. Scott From the Program in Stem Cell Biology and Regenerative Medicine, University of Florida Shand's Cancer Center, Gainesville, FL. We have previously established a model inducing hematopoietic stem cell (HSC) production of circulating endothelial progenitor cells (EPCs) to revascularize ischemic injury in adult mouse retina. The unique vascular environment of the retina results in new blood vessel formation primarily from HSC-derived EPCs. Using mice deficient (–/–) in inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS), we show that vessel phenotype resulting from hemangioblast activity can be altered by modulation of the NO/NOS pathway. iNOS–/– or eNOS–/– animals were engrafted with wild-type (WT) HSCs expressing green fluorescence protein (gfp+) and subjected to our adult retinal ischemia model. WT hemangioblast activity in adult iNOS–/– recipients resulted in the formation of highly branched blood vessels of donor origin, which were readily perfused indicating functionality. In contrast, eNOS–/– recipients produced relatively unbranched blood vessels with significant donor contribution that were difficult to perfuse, indicating poor functionality. Furthermore, eNOS–/– chimeras had extensive gfp+ HSC contribution throughout their vasculature without additional injury. This neovascularization, via EPCs derived from the transplanted HSCs, reveals that the NO pathway can modulate EPC activity and plays a critical role in both blood vessel formation in response to injury and normal endothelial cell maintenance. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: NO role in EPC function Mervin C. Yoder Blood 2005 105: 1846-1847. [Full Text] [PDF] This article has been cited by other articles: C. Baylis Nitric oxide deficiency in chronic kidney disease Am J Physiol Renal Physiol, January 1, 2008; 294(1): F1 - F9. [Abstract] [Full Text] [PDF] A. Schmidt, K. Brixius, and W. Bloch Endothelial Precursor Cell Migration During Vasculogenesis Circ. Res., July 20, 2007; 101(2): 125 - 136. [Abstract] [Full Text] [PDF] Y. Kanetsuna, K. Takahashi, M. Nagata, M. A. Gannon, M. D. Breyer, R. C. Harris, and T. 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