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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.
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Submitted September 9, 2004
Accepted October 24, 2004
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*
Program in Stem Cell Biology and Regenerative Medicine, University of Florida Shand's Cancer Center, Gainesville, FL, USA
* Corresponding author; email: escott{at}ufl.edu.
We have previously established a model inducing hematopoietic stem cell (HSC) production of circulating endothelial progenitor cells (EPC) 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 EPC. Using inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) deficient (-/-) mice, we show that vessel phenotype resulting from hemangioblast activity can be altered by modulation of the nitric oxide/nitric oxide synthase pathway. iNOS-/- or eNOS-/- animals were engrafted with wild type (WT) HSC 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 EPC derived from the transplanted HSC, 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.
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