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• W2055199717 abstract "During embryonic development, the vasculature is among the first organs to form and is in charge of maintaining metabolic homeostasis by supplying oxygen and nutrients and removing waste products. As one would expect, blood vessels are critical not only for organ growth in the embryo but also for repair of wounded tissue in the adult. An imbalance in angiogenesis (a time-honored term that globally refers to the growth of new blood vessels) contributes to the pathogenesis of numerous malignant, inflammatory, ischemic, infectious, immune, and wound-healing disorders. This review focuses on the central role of the growth of new blood vessels in ischemic and diabetic wound healing and defines the most current nomenclature that describes the neovascularization process in wounds. There are now two well-defined, distinct, yet interrelated processes for the formation of postnatal new blood vessels, angiogenesis, and vasculogenesis. Reviewed are recent new data on vasculogenesis that promise to advance the field of wound healing. During embryonic development, the vasculature is among the first organs to form and is in charge of maintaining metabolic homeostasis by supplying oxygen and nutrients and removing waste products. As one would expect, blood vessels are critical not only for organ growth in the embryo but also for repair of wounded tissue in the adult. An imbalance in angiogenesis (a time-honored term that globally refers to the growth of new blood vessels) contributes to the pathogenesis of numerous malignant, inflammatory, ischemic, infectious, immune, and wound-healing disorders. This review focuses on the central role of the growth of new blood vessels in ischemic and diabetic wound healing and defines the most current nomenclature that describes the neovascularization process in wounds. There are now two well-defined, distinct, yet interrelated processes for the formation of postnatal new blood vessels, angiogenesis, and vasculogenesis. Reviewed are recent new data on vasculogenesis that promise to advance the field of wound healing. It is now well established that an essential part of normal healing for full thickness cutaneous wounds is the formation of new blood vessels within the provisional wound matrix that is referred to as granulation tissue. Neovascularization of the wound’s granulation tissue occurs by the processes of angiogenesis or vasculogenesis, or both.1Bauer S.M. Bauer R.J. Velazquez O.C. Angiogenesis, vasculogenesis, and induction of healing in chronic wounds.Vasc Endovascular Surg. 2005; 39: 293-306Crossref PubMed Scopus (169) Google Scholar Angiogenesis refers to the process by which resident endothelial cells of the wound’s adjacent mature vascular network proliferate, migrate, and remodel into neovessels that grow into the initially avascular wound tissue aided by mature stromal cells such as fibroblasts.1Bauer S.M. Bauer R.J. Velazquez O.C. Angiogenesis, vasculogenesis, and induction of healing in chronic wounds.Vasc Endovascular Surg. 2005; 39: 293-306Crossref PubMed Scopus (169) Google Scholar, 2Hanahan D. Signaling vascular morphogenesis and maintenance.Science. 1997; 277: 48-50Crossref PubMed Scopus (1019) Google Scholar, 3Carmeliet P. Mechanisms of angiogenesis and arteriogenesis.Nat Med. 2000; 6: 389-395Crossref PubMed Scopus (3320) Google Scholar, 4Velazquez O.C. Snyder R. Liu Z.J. Fairman R.M. Herlyn M. Fibroblast-dependent differentiation of human microvascular endothelial cells into capillary-like 3-dimensional networks.FASEB J. 2002; 16: 1316-1318Crossref PubMed Scopus (108) Google Scholar, 5Liu Z.J. Snyder R. Soma A. Shirakawa T. Ziober B.L. Fairman R.M. et al.VEGF-A and alphaVbeta3 integrin synergistically rescue angiogenesis via N-Ras and PI3-K signaling in human microvascular endothelial cells.FASEB J. 2003; 17: 1931-1933PubMed Google Scholar, 6Bauer S.M. Bauer R.J. Liu Z.J. Chen H. Goldstein L. Velazquez O.C. Vascular endothelial growth factor-C promotes vasculogenesis, angiogenesis, and collagen constriction in three-dimensional collagen gels.J Vasc Surg. 2005; 41: 699-707Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar Vasculogenesis is a de novo process by which progenitor stem cells differentiate and give rise to a replacement vascular network.7Tepper O.M. Capla J.M. Galiano R.D. Ceradini D.J. Callaghan M.J. Kleinman M.E. et al.Adult vasculogenesis occurs through the in situ recruitment, proliferation and tubulization of circulating bone marrow-derived cells.Blood. 2005; 105: 1068-1077Crossref PubMed Scopus (379) Google Scholar, 8Reyes M. Dudek A. Jahagirdar B. Koodie L. Marker P.H. Verfaillie C.M. Origin of endothelial progenitors in human postnatal bone marrow.J Clin Invest. 2002; 109: 337-346Crossref PubMed Scopus (1102) Google Scholar, 9Takahashi T. Kalka C. Masuda H. Chen D. Silver M. Kearney M. et al.Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization.Nat Med. 1999; 5: 434-438Crossref PubMed Scopus (46) Google Scholar It was once believed that vasculogenesis only occurred during embryonic life; however, bone marrow-derived endothelial progenitor cells (BMD EPCs) have been identified in peripheral blood in adults and participate in new vessel formation.7Tepper O.M. Capla J.M. Galiano R.D. Ceradini D.J. Callaghan M.J. Kleinman M.E. et al.Adult vasculogenesis occurs through the in situ recruitment, proliferation and tubulization of circulating bone marrow-derived cells.Blood. 2005; 105: 1068-1077Crossref PubMed Scopus (379) Google Scholar, 10Asahara T. Takahashi T. Masuda H. Kalka C. Chen D. Iwaguro H. et al.VEGF contributes to postnatal neovascularization by mobilizing bone marrow-derived endothelial progenitor cells.Embo J. 1999; 18: 3964-3972Crossref PubMed Scopus (1626) Google Scholar BMD EPCs contribute to wound healing because these progenitor/stem cells are the key cellular effectors of postnatal vasculogenesis. BMD EPCs given to animals with surgically induced limb ischemia incorporate into foci of neovascularization in ischemic muscle, skin, and wounds.7Tepper O.M. Capla J.M. Galiano R.D. Ceradini D.J. Callaghan M.J. Kleinman M.E. et al.Adult vasculogenesis occurs through the in situ recruitment, proliferation and tubulization of circulating bone marrow-derived cells.Blood. 2005; 105: 1068-1077Crossref PubMed Scopus (379) Google Scholar, 8Reyes M. Dudek A. Jahagirdar B. Koodie L. Marker P.H. Verfaillie C.M. Origin of endothelial progenitors in human postnatal bone marrow.J Clin Invest. 2002; 109: 337-346Crossref PubMed Scopus (1102) Google Scholar, 9Takahashi T. Kalka C. Masuda H. Chen D. Silver M. Kearney M. et al.Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization.Nat Med. 1999; 5: 434-438Crossref PubMed Scopus (46) Google Scholar, 10Asahara T. Takahashi T. Masuda H. Kalka C. Chen D. Iwaguro H. et al.VEGF contributes to postnatal neovascularization by mobilizing bone marrow-derived endothelial progenitor cells.Embo J. 1999; 18: 3964-3972Crossref PubMed Scopus (1626) Google Scholar, 11Kalka C. Masuda H. Takahashi T. Kalka-Moll W.M. Silver M. Kearney M. et al.Transplantation of ex vivo expanded endothelial progenitor cells for therapeutic neovascularization.Proc Natl Acad Sci U S A. 2000; 97: 3422-3427Crossref PubMed Scopus (1737) Google Scholar, 12Shintani S. Murohara T. Ikeda H. Ueno T. Honma T. Katoh A. et al.Mobilization of endothelial progenitor cells in patients with acute myocardial infarction.Circulation. 2001; 103: 2776-2779Crossref PubMed Scopus (1027) Google Scholar, 13Kawamoto A. Gwon H.C. Iwaguro H. Yamaguchi J.I. Uchida S. Masuda H. et al.Therapeutic potential of ex vivo expanded endothelial progenitor cells for myocardial ischemia.Circulation. 2001; 103: 634-637Crossref PubMed Scopus (1101) Google Scholar We have recently identified a critical role for BMD EPCs in ischemic wound healing.14Bauer S.M. Goldstein L.J. Bauer R.J. Chen H. Putt M. Velazquez O.C. The bone marrow-derived endothelial progenitor cell response is impaired in delayed wound healing from ischemia.J Vasc Surg. 2006; 43: 134-141Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar We quantified the contribution of BMD EPCs to wound healing with and without ischemia in chimeric mice formed using bone marrow from FVB/Tie-2-LacZ transgenic mice (FVB/N-TgN[TIE2LacZ]182Sato, The Jackson Laboratory, Bar Harbor, Me). Tie-2-LacZ mice are well suited for specifically tracking BMD PCs of the endothelial cell lineage because the endothelial-specific Tie-2 promoter is linked to the LacZ reporter gene allowing cells to be identified by β-galactosidase (β-gal) expression. We used a murine model of hind limb ischemia induced by femoral ligation/excision (Fig 1) in the chimeric mice we created (Fig 2, A). Hind limb ischemia was monitored using laser Doppler flowmetry that allows for quantifying cutaneous blood flow in the ischemic relative to the nonischemic hind limb. Hind limb ischemia resulted in delayed wound healing (Fig 2, A-C). We then compared acutely healing wounds in nonischemic hind limbs with delayed healing wounds in the contralateral ischemic hind limb and correlated healing rates to BMD EPC recruitment into wounds. We determined that BMD EPCs play a key role in wound healing and are recruited into the granulation tissue of rapidly healing (nonischemic) wounds in significantly greater numbers than into delayed-healing (ischemic) wounds (Fig 2, D-G). These studies show that BMD EPCs contribute to acute wound healing, and the process is deficient or incomplete at the level of skin wounds in the presence of severe ischemia.14Bauer S.M. Goldstein L.J. Bauer R.J. Chen H. Putt M. Velazquez O.C. The bone marrow-derived endothelial progenitor cell response is impaired in delayed wound healing from ischemia.J Vasc Surg. 2006; 43: 134-141Abstract Full Text Full Text PDF PubMed Scopus (68) Google ScholarFig 2Bone marrow–derived endothelial progenitor cells (EPC) recruited to wounds. A, The model. B, Delay in healing in ischemic wound (IW) vs rapid healing in nonischemic wound (NIW). C, Wound closure rates (n = 7 per time point) are shown with mean ± standard error in ischemic (triangles) and nonischemic (squares) wounds. D, Quantification of EPCs in wounds (ischemic, diamonds; nonischemic, triangle) and underlying muscle (nonischemic, squares; ischemic, plain) shows increased EPCs in acutely healing nonischemic wounds at days 3 and 7 (data presented as mean ± standard error). E, F, Representative wounds at day 3 (EPCs are β-Gal+ cells seen staining blue). G, EPCs per high power fields (HPF) in wound, underlying muscle, adjacent skin, and remote skin at day 3 after wounding (data presented as mean ± standard error). (Data and modified figure reprinted with permission from Bauer et al.14Bauer S.M. Goldstein L.J. Bauer R.J. Chen H. Putt M. Velazquez O.C. The bone marrow-derived endothelial progenitor cell response is impaired in delayed wound healing from ischemia.J Vasc Surg. 2006; 43: 134-141Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar)View Large Image Figure ViewerDownload Hi-res image Download (PPT) In diabetic patients and diabetic murine models, the number and function of circulating BMD EPCs is severely impaired, and this defect is highly correlated with the long-term cardiovascular and wound-healing complications seen in diabetes mellitus.15Keswani S.G. Katz A.B. Lim F.Y. Zoltick P. Radu A. Alaee D. et al.Adenoviral mediated gene transfer of PDGF-B enhances wound healing in type I and type II diabetic wounds.Wound Repair Regen. 2004; 12: 497-504Crossref PubMed Scopus (99) Google Scholar, 16Fadini G.P. Miorin M. Facco M. Bonamico S. Baesso I. Grego F. et al.Circulating endothelial progenitor cells are reduced in peripheral vascular complications of type 2 diabetes mellitus.J Am Coll Cardiol. 2005; 45: 1449-1457Abstract Full Text Full Text PDF PubMed Scopus (596) Google Scholar, 17Tepper O.M. Galiano R.D. Capla J.M. Kalka C. Gagne P.J. Jacobowitz G.R. et al.Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures.Circulation. 2002; 106: 2781-2786Crossref PubMed Scopus (1259) Google Scholar, 18Loomans C.J. de Koning E.J. Staal F.J. Rookmaaker M.B. Verseyden C. de Boer H.C. et al.Endothelial progenitor cell dysfunction: a novel concept in the pathogenesis of vascular complications of type 1 diabetes.Diabetes. 2004; 53: 195-199Crossref PubMed Scopus (737) Google Scholar, 19Vasa M. Fichtlscherer S. Aicher A. Adler K. Urbich C. Martin H. et al.Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease.Circ Res. 2001; 89: E1-E7Crossref PubMed Scopus (2045) Google Scholar Increasing evidence suggests that wound-healing mechanisms, in both the bone marrow and within the peripheral wound, are compromised by diabetes as a result of BMD EPC impairments.15Keswani S.G. Katz A.B. Lim F.Y. Zoltick P. Radu A. Alaee D. et al.Adenoviral mediated gene transfer of PDGF-B enhances wound healing in type I and type II diabetic wounds.Wound Repair Regen. 2004; 12: 497-504Crossref PubMed Scopus (99) Google Scholar, 16Fadini G.P. Miorin M. Facco M. Bonamico S. Baesso I. Grego F. et al.Circulating endothelial progenitor cells are reduced in peripheral vascular complications of type 2 diabetes mellitus.J Am Coll Cardiol. 2005; 45: 1449-1457Abstract Full Text Full Text PDF PubMed Scopus (596) Google Scholar, 17Tepper O.M. Galiano R.D. Capla J.M. Kalka C. Gagne P.J. Jacobowitz G.R. et al.Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures.Circulation. 2002; 106: 2781-2786Crossref PubMed Scopus (1259) Google Scholar, 18Loomans C.J. de Koning E.J. Staal F.J. Rookmaaker M.B. Verseyden C. de Boer H.C. et al.Endothelial progenitor cell dysfunction: a novel concept in the pathogenesis of vascular complications of type 1 diabetes.Diabetes. 2004; 53: 195-199Crossref PubMed Scopus (737) Google Scholar, 19Vasa M. Fichtlscherer S. Aicher A. Adler K. Urbich C. Martin H. et al.Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease.Circ Res. 2001; 89: E1-E7Crossref PubMed Scopus (2045) Google Scholar, 20Loomans C.J. De Koning E.J. Staal F.J. Rabelink T.J. Zonneveld A.J. Endothelial progenitor cell dysfunction in type 1 diabetes: another consequence of oxidative stress?.Antioxid Redox Signal. 2005; 7: 1468-1475Crossref PubMed Scopus (58) Google Scholar Although cytokines such as granulocyte colony-stimulating factor (GM-CSF) and growth factors such as vascular endothelial growth factor-A (VEGF-A) can induce the release of progenitor cells from the bone marrow, the nonspecific effects on release of other white cells and platelets or the leaky-capillary effect has made these factors unsuitable to treat diabetic patients with nonhealing chronic wounds.21Li B. Ogasawara A.K. Yang R. Wei W. He G.W. Zioncheck T.F. et al.KDR (VEGF receptor 2) is the major mediator for the hypotensive effect of VEGF.Hypertension. 2002; 39: 1095-1100Crossref PubMed Scopus (100) Google Scholar, 22Kawachi Y. Watanabe A. Uchida T. Yoshizawa K. Kurooka N. Setsu K. Acute arterial thrombosis due to platelet aggregation in a patient receiving granulocyte colony-stimulating factor.Br J Haematol. 1996; 94: 413-416Crossref PubMed Scopus (73) Google Scholar, 23Tolcher A.W. Giusti R.M. O’Shaughnessy J.A. Cowan K.H. Arterial thrombosis associated with granulocyte-macrophage colony-stimulating factor (GM-CSF) administration in breast cancer patients treated with dose-intensive chemotherapy: a report of two cases.Cancer Invest. 1995; 13: 188-192Crossref PubMed Scopus (28) Google Scholar, 24Fukumoto Y. Miyamoto T. Okamura T. Gondo H. Iwasaki H. Horiuchi T. et al.Angina pectoris occurring during granulocyte colony-stimulating factor-combined preparatory regimen for autologous peripheral blood stem cell transplantation in a patient with acute myelogenous leukaemia.Br J Haematol. 1997; 97: 666-668Crossref PubMed Scopus (59) Google Scholar, 25Lindemann A. Rumberger B. Vascular complications in patients treated with granulocyte colony-stimulating factor (G-CSF).Eur J Cancer. 1993; 29A: 2338-2339Abstract Full Text PDF PubMed Scopus (45) Google Scholar Systemic hyperoxia induced by hyperbaric oxygen (HBO2) is a treatment approved by the United States Food and Drug Administration (FDA) as a safe, adjunctive therapy to stimulate wound healing in diabetic patients. Patients typically receive ≥20 treatments with pure oxygen at 2.0 to 2.4 atmospheres absolute (ATA) once or twice daily. Controlled trials have shown efficacy for HBO2 in refractory diabetic wounds, but the mechanisms of action are poorly understood.26Abidia A. Laden G. Kuhan G. Johnson B.F. Wilkinson A.R. Renwick P.M. et al.The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomised-controlled trial.Eur J Vasc Endovasc Surg. 2003; 25: 513-518Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar, 27Baroni G. Porro T. Faglia E. Pizzi G. Mastropasqua A. Oriani G. et al.Hyperbaric oxygen in diabetic gangrene treatment.Diabetes Care. 1987; 10: 81-86Crossref PubMed Scopus (136) Google Scholar, 28Doctor N. Pandya S. Supe A. Hyperbaric oxygen therapy in diabetic foot.J Postgrad Med. 1992; 38 (111): 112-114PubMed Google Scholar, 29Faglia E. Favales F. Aldeghi A. Calia P. Quarantiello A. Oriani G. et al.Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer A randomized study.Diabetes Care. 1996; 19: 1338-1343Crossref PubMed Scopus (319) Google Scholar, 30Kalani M. Jorneskog G. Naderi N. Lind F. Brismar K. Hyperbaric oxygen (HBO) therapy in treatment of diabetic foot ulcers Long-term follow-up.J Diabetes Complications. 2002; 16: 153-158Abstract Full Text Full Text PDF PubMed Scopus (183) Google Scholar, 31Zamboni W.A. Wong H.P. Stephenson L.L. Pfeifer M.A. Evaluation of hyperbaric oxygen for diabetic wounds: a prospective study.Undersea Hyperb Med. 1997; 24: 175-179PubMed Google Scholar HBO2 is not uniformly effective, particularly in diabetic patients with associated peripheral arterial disease (PAD), accounting for the fact that diabetic/ischemic chronic nonhealing lower extremity wounds continue to be an unsolved clinical problem. Recent investigations from our laboratory indicate that hyperoxia therapeutically stimulates progenitor/stem cell release from the bone marrow, but these cells may be effectively recruited to wounds to enhance vasculogenesis and healing only if the cytokine milieu in the cutaneous wound bed is optimized.32Thom S.R. Bhopale V.M. Velazquez O.C. Goldstein L.J. Thom L.H. Buerk D.G. Stem cell mobilization by hyperbaric oxygen.Am J Physiol Heart Circ Physiol. 2006; 290: H1378-H1386Crossref PubMed Scopus (214) Google Scholar, 33Goldstein L.J. Gallagher K.A. Bauer S.M. Bauer R.J. Baireddy V. Liu Z.J. et al.Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide.Stem Cells. 2006; 24: 2309-2318Crossref PubMed Scopus (111) Google Scholar, 34Gallagher K.A. Goldstein L.J. Thom S.R. Velazquez O.C. Hyperbaric oxygen and bone marrow–derived endothelial progenitor cells in diabetic wound healing.Vascular. 2006; 14: 328-337Crossref PubMed Scopus (62) Google Scholar Using ischemic and diabetic murine models, we have recently determined that hyperoxia, induced by a clinically relevant HBO2 protocol, increases nitric oxide (NO) levels within femoral bone marrow, accelerates the spontaneous revascularization of surgically induced hind limb ischemia, and increases the number of BMD PCs in circulation and within cutaneous hind limb ischemic incisional wounds and diabetic excisional wounds.33Goldstein L.J. Gallagher K.A. Bauer S.M. Bauer R.J. Baireddy V. Liu Z.J. et al.Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide.Stem Cells. 2006; 24: 2309-2318Crossref PubMed Scopus (111) Google Scholar, 34Gallagher K.A. Goldstein L.J. Thom S.R. Velazquez O.C. Hyperbaric oxygen and bone marrow–derived endothelial progenitor cells in diabetic wound healing.Vascular. 2006; 14: 328-337Crossref PubMed Scopus (62) Google Scholar These effects appear to be specific to the release of BMD EPC and responsive to the cytokine milieu of the wound.33Goldstein L.J. Gallagher K.A. Bauer S.M. Bauer R.J. Baireddy V. Liu Z.J. et al.Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide.Stem Cells. 2006; 24: 2309-2318Crossref PubMed Scopus (111) Google Scholar, 34Gallagher K.A. Goldstein L.J. Thom S.R. Velazquez O.C. Hyperbaric oxygen and bone marrow–derived endothelial progenitor cells in diabetic wound healing.Vascular. 2006; 14: 328-337Crossref PubMed Scopus (62) Google Scholar In the ischemic and diabetic murine models that were used, therapeutic wound-healing effects of increased BMD EPC mobilization into circulation and recruitment into wounds were observed in association with enhancement of neovascularization of the wounds and spontaneous recovery of hind limb perfusion.33Goldstein L.J. Gallagher K.A. Bauer S.M. Bauer R.J. Baireddy V. Liu Z.J. et al.Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide.Stem Cells. 2006; 24: 2309-2318Crossref PubMed Scopus (111) Google Scholar, 34Gallagher K.A. Goldstein L.J. Thom S.R. Velazquez O.C. Hyperbaric oxygen and bone marrow–derived endothelial progenitor cells in diabetic wound healing.Vascular. 2006; 14: 328-337Crossref PubMed Scopus (62) Google Scholar It is increasingly evident that wound healing occurs because of events in two compartments. Within the bone marrow, various signaling pathways lead to mobilization of BMD EPCs and other progenitor/stem cells involved in the healing cascade. Within the wound, neovascularization occurs because of local factors that stimulate adjacent cells (angiogenesis) and because of recruited circulating BMD EPCs that contribute to existing and new vascular channels (vasculogenesis). Vascular maintenance, repair, and wound-healing cellular and molecular cascades at the level of both the bone marrow and within the peripheral wound are compromised by diabetes as a result of BMD EPC impairments.15Keswani S.G. Katz A.B. Lim F.Y. Zoltick P. Radu A. Alaee D. et al.Adenoviral mediated gene transfer of PDGF-B enhances wound healing in type I and type II diabetic wounds.Wound Repair Regen. 2004; 12: 497-504Crossref PubMed Scopus (99) Google Scholar, 16Fadini G.P. Miorin M. Facco M. Bonamico S. Baesso I. Grego F. et al.Circulating endothelial progenitor cells are reduced in peripheral vascular complications of type 2 diabetes mellitus.J Am Coll Cardiol. 2005; 45: 1449-1457Abstract Full Text Full Text PDF PubMed Scopus (596) Google Scholar, 17Tepper O.M. Galiano R.D. Capla J.M. Kalka C. Gagne P.J. Jacobowitz G.R. et al.Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures.Circulation. 2002; 106: 2781-2786Crossref PubMed Scopus (1259) Google Scholar, 18Loomans C.J. de Koning E.J. Staal F.J. Rookmaaker M.B. Verseyden C. de Boer H.C. et al.Endothelial progenitor cell dysfunction: a novel concept in the pathogenesis of vascular complications of type 1 diabetes.Diabetes. 2004; 53: 195-199Crossref PubMed Scopus (737) Google Scholar, 19Vasa M. Fichtlscherer S. Aicher A. Adler K. Urbich C. Martin H. et al.Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease.Circ Res. 2001; 89: E1-E7Crossref PubMed Scopus (2045) Google Scholar, 20Loomans C.J. De Koning E.J. Staal F.J. Rabelink T.J. Zonneveld A.J. Endothelial progenitor cell dysfunction in type 1 diabetes: another consequence of oxidative stress?.Antioxid Redox Signal. 2005; 7: 1468-1475Crossref PubMed Scopus (58) Google Scholar The use of cytokines and growth factors such as GM-CSF and VEGF-A to stimulate the bone marrow release of progenitor stem cells for purposes such as wound healing or therapeutic neovascularization has been considered, but generalized application has been thwarted because of risks such as acute arterial thrombosis, angina, hypotension, sepsis, and death.21Li B. Ogasawara A.K. Yang R. Wei W. He G.W. Zioncheck T.F. et al.KDR (VEGF receptor 2) is the major mediator for the hypotensive effect of VEGF.Hypertension. 2002; 39: 1095-1100Crossref PubMed Scopus (100) Google Scholar, 22Kawachi Y. Watanabe A. Uchida T. Yoshizawa K. Kurooka N. Setsu K. Acute arterial thrombosis due to platelet aggregation in a patient receiving granulocyte colony-stimulating factor.Br J Haematol. 1996; 94: 413-416Crossref PubMed Scopus (73) Google Scholar, 23Tolcher A.W. Giusti R.M. O’Shaughnessy J.A. Cowan K.H. Arterial thrombosis associated with granulocyte-macrophage colony-stimulating factor (GM-CSF) administration in breast cancer patients treated with dose-intensive chemotherapy: a report of two cases.Cancer Invest. 1995; 13: 188-192Crossref PubMed Scopus (28) Google Scholar, 24Fukumoto Y. Miyamoto T. Okamura T. Gondo H. Iwasaki H. Horiuchi T. et al.Angina pectoris occurring during granulocyte colony-stimulating factor-combined preparatory regimen for autologous peripheral blood stem cell transplantation in a patient with acute myelogenous leukaemia.Br J Haematol. 1997; 97: 666-668Crossref PubMed Scopus (59) Google Scholar, 25Lindemann A. Rumberger B. Vascular complications in patients treated with granulocyte colony-stimulating factor (G-CSF).Eur J Cancer. 1993; 29A: 2338-2339Abstract Full Text PDF PubMed Scopus (45) Google Scholar, 35To L.B. Haylock D.N. Simmons P.J. Juttner C.A. The biology and clinical uses of blood stem cells.Blood. 1997; 89: 2233-2258Crossref PubMed Google Scholar Overall, normal cutaneous wound healing proceeds through an orderly sequence of steps that require the control of contamination and infection, resolution of inflammation, regeneration of the connective tissue matrix, angiogenesis/vasculogenesis, wound constriction, and re-epithelialization. Chronic wounds are those that have failed to follow this sequence and do not achieve a sustained anatomic and functional result.36Lazarus G.S. Cooper D.M. Knighton D.R. Margolis D.J. Pecoraro R.E. Rodeheaver G. et al.Definitions and guidelines for assessment of wounds and evaluation of healing.Arch Dermatol. 1994; 130: 489-493Crossref PubMed Scopus (529) Google Scholar The hypoxic nature of all wounds has been demonstrated, but when hypoxia is pathologically increased, wound healing is impaired and the rate of wound infection increases.35To L.B. Haylock D.N. Simmons P.J. Juttner C.A. The biology and clinical uses of blood stem cells.Blood. 1997; 89: 2233-2258Crossref PubMed Google Scholar, 36Lazarus G.S. Cooper D.M. Knighton D.R. Margolis D.J. Pecoraro R.E. Rodeheaver G. et al.Definitions and guidelines for assessment of wounds and evaluation of healing.Arch Dermatol. 1994; 130: 489-493Crossref PubMed Scopus (529) Google Scholar, 37Ceradini D.J. Kulkarni A.R. Callaghan M.J. Tepper O.M. Bastidas N. 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Measuring tissue oxygen tension: a review.Undersea Hyperb Med. 1998; 25: 179-188PubMed Google Scholar Fibroblast replication, collagen deposition, angiogenesis, vasculogenesis, and intracellular leukocyte bacterial killing are oxygen-sensitive responses essential to wound healing.33Goldstein L.J. Gallagher K.A. Bauer S.M. Bauer R.J. Baireddy V. Liu Z.J. et al.Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide.Stem Cells. 2006; 24: 2309-2318Crossref PubMed Scopus (111) Google Scholar, 34Gallagher K.A. Goldstein L.J. Thom S.R. Velazquez O.C. Hyperbaric oxygen and bone marrow–derived endothelial progenitor cells in diabetic wound healing.Vascular. 2006; 14: 328-337Crossref PubMed Scopus (62) Google Scholar, 39Hunt T.K. Pai M.P. The effect of varying ambient oxygen tensions on wound metabolism and collagen synthesis.Surg Gynecol Obstet. 1972; 135: 561-567PubMed Google Scholar, 42LaVan F.B. Hunt T.K. 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• W2055199717 created "2016-06-24" @default.
• W2055199717 creator A5033528741 @default.
• W2055199717 date "2007-06-01" @default.
• W2055199717 modified "2023-10-12" @default.
• W2055199717 title "Angiogenesis and vasculogenesis: Inducing the growth of new blood vessels and wound healing by stimulation of bone marrow–derived progenitor cell mobilization and homing" @default.
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• W2055199717 doi "https://doi.org/10.1016/j.jvs.2007.02.068" @default.
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