{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T12:39:05Z","timestamp":1772195945305,"version":"3.50.1"},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2008,12,8]],"date-time":"2008-12-08T00:00:00Z","timestamp":1228694400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Metabolism Res"],"published-print":{"date-parts":[[2009,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Endothelial progenitor cells (EPCs) in bone marrow (BM) and peripheral blood (PB) contribute to tissue repair in various pathological conditions <jats:italic>via<\/jats:italic> the formation of new blood vessels. Previous studies indicate that diabetic patients have reduced EPC number and deregulated EPC function, although the regenerative properties of EPCs in diabetes are unknown. We wish to characterize and compare EPCs from pre\u2010diabetic and diabetic non\u2010obese diabetic (NOD) mice, a model of type 1 diabetes (T1D), in order to delineate the role of these cells in the pathogenesis of autoimmune diabetes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Whole BM was obtained by flushing femurs, tibias and illiac crests from pre\u2010diabetic and diabetic NOD mice (5\u201330 weeks) in which the diabetic status was confirmed by measuring blood glucose levels (\u226511.5 mmol\/L); PB was collected in heparin\u2010coated tubes and lysed after incubation with antibodies directed against EPCs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>FACS analyses revealed a significant decrease in EPC number (CD31<jats:sup>+<\/jats:sup>, c\u2010Kit<jats:sup>+<\/jats:sup>, Sca\u20101<jats:sup>+<\/jats:sup>, Lin<jats:sup>\u2212<\/jats:sup>) in BM from diabetic compared to pre\u2010diabetic mice (<jats:italic>P<\/jats:italic> = 0.02). Conversely, EPC number was significantly increased in PB from diabetic compared to pre\u2010diabetic mice (<jats:italic>P<\/jats:italic> = 0.01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These data suggest that at the onset of diabetes, BM\u2010derived EPCs are stimulated to enter the systemic circulation likely in response to signals from the pancreas. Further studies are required to elucidate whether EPCs home the damaged pancreas, thus representing a prospective source of autologous cells for \u03b2\u2010cell regeneration therapy. Copyright \u00a9 2008 John Wiley &amp; Sons, Ltd.<\/jats:p><\/jats:sec>","DOI":"10.1002\/dmrr.898","type":"journal-article","created":{"date-parts":[[2008,12,9]],"date-time":"2008-12-09T21:26:32Z","timestamp":1228857992000},"page":"89-93","source":"Crossref","is-referenced-by-count":8,"title":["Characterization of endothelial progenitor cells in the NOD mouse as a source for cell therapies"],"prefix":"10.1002","volume":"25","author":[{"given":"Cheen Peen","family":"Khoo","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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