Journal articles: 'Circulating progenitor cells'

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Anversa, Piero, Jan Kajstura, and Annarosa Leri. "Circulating Progenitor Cells." Circulation 110, no. 20 (November 16, 2004): 3158–60. http://dx.doi.org/10.1161/01.cir.0000148679.30170.78.

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Schwartzenberg, Shmuel, Varda Deutsch, Sofia Maysel-Auslender, Sarina Kissil, Gad Keren, and Jacob George. "Circulating Apoptotic Progenitor Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 5 (May 2007): 1079. http://dx.doi.org/10.1161/atvb.27.5.1079.

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Garmy-Susini, B., and J. A. Varner. "Circulating endothelial progenitor cells." British Journal of Cancer 93, no. 8 (September 27, 2005): 855–58. http://dx.doi.org/10.1038/sj.bjc.6602808.

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Susini, Sandrine, Séverine Mouraud, Elodie Elkaim, Julien Roullier, Sonia Luce, Olivier Pellé, Julie Bruneau, Marina Cavazzana, and Isabelle Andre-Schmutz. "From the Bone Marrow to the Thymic Niche." Blood 124, no. 21 (December 6, 2014): 5123. http://dx.doi.org/10.1182/blood.v124.21.5123.5123.

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Abstract To generate T cells throughout adult life, the thymus must import hematopoietic progenitor cells from the bone marrow via the blood. The cellular and molecular mechanisms governing the circulation of thymus-seeding progenitor cells are well characterized in mice but not in humans. The aim of the present study was to characterize the molecular mechanisms and cellular components involved in thymus colonization by lymphoid progenitors (CD34+/CD10+/CD7-/CD24-) and the early steps of thymopoiesis under physiological conditions in humans. Our results demonstrate that circulating lymphoid progenitor cells express CCR9 and CXCR4 chemokine receptors, VLA-4, VLA-5 and VLA-6 integrins and PSGL-1 and CD44 adhesion molecules. We used in vitro migration and adhesion assays to validate the functional status of these markers. As in the mouse, human circulating progenitor cells enter the thymus at the corticomedullary junction (CMJ). Once in the thymus, crosstalk with thymic epithelial cells causes the circulating progenitors to commit to the T-cell differentiation pathway. In order to characterize thymic niches and interactions between circulating progenitors and the thymic stroma, we undertook a chemokine/chemokine-receptor-focused gene expression analysis of sorted lymphoid progenitor cells and CMJ epithelial cells (based on the expression of EpCAM and Delta-like-4). We observed an unexpected gene expression profile for chemokines and chemokine regulators in thymus-seeding CD34+/CD10+/CD7-/CD24- cells and epithelial cells at the CMJ. The present results should help us to highlight candidate genes involved in the early steps of human thymopoiesis. Disclosures No relevant conflicts of interest to declare.

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Gomer, Richard H. "Circulating progenitor cells and scleroderma." Current Rheumatology Reports 10, no. 3 (June 2008): 183–88. http://dx.doi.org/10.1007/s11926-008-0031-8.

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Díaz del Moral, Sandra, Silvia Barrena, Ramón Muñoz-Chápuli, and Rita Carmona. "Embryonic circulating endothelial progenitor cells." Angiogenesis 23, no. 4 (July 1, 2020): 531–41. http://dx.doi.org/10.1007/s10456-020-09732-y.

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Wang, Chunlin, Chunhua Jiao, Heather D. Hanlon, Wei Zheng, Robert J. Tomanek, and Gina C. Schatteman. "Mechanical, cellular, and molecular factors interact to modulate circulating endothelial cell progenitors." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1985—H1993. http://dx.doi.org/10.1152/ajpheart.00431.2003.

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It appears that there are two classes of human circulating endothelial cell (EC) progenitors, CD34+and CD34–CD14+cells. Attention has focused on CD34+cells, yet CD34–CD14+monocytic cells are far more abundant and may represent the most common class of circulating EC progenitor. Little is known about molecular or physiological factors that regulate putative CD34–CD14+EC progenitor function, although factors secreted by other blood and cardiovascular cells to which they are exposed probably affect their behavior. Hypoxia and stretch are two important physiological stimuli known to trigger growth factors in cardiovascular cells and accordingly may modulate EC progenitors. To investigate the impact of these environmental parameters on EC progenitors, EC production in CD34–CD14+cultures was evaluated. Our data indicate that neither stretch nor hypoxia alters EC production by EC progenitors directly but do so indirectly through their effects on cardiovascular cells. Conditioned media (CM) from coronary artery smooth muscle cells inhibit EC production in culture, and this inhibition is stronger if the coronary smooth muscle cells have been subjected to cyclic stretch. In contrast, cardiomyocyte CM increases EC cell number, an effect that is potentiated if the myocytes have been subjected to hypoxia. Significantly, EC progenitor responses to CM are altered by the presence of CD34–CD14–peripheral blood mononuclear cells (PBMCs). Moreover, CD34–CD14–PBMCs attenuate EC progenitor responsiveness to the angiogenic factors basic fibroblast growth factor (FGF-2), vascular endothelial cell growth factor-A165, and erythropoietin while inducing EC progenitor death in the presence of transforming growth factor-β1in vitro

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Jönsson, Daniel, Thomas Spinell, Anastasios Vrettos, Christin Stoecklin-Wasmer, Romanita Celenti, Ryan T. Demmer, Moritz Kebschull, and Panos N. Papapanou. "Circulating Endothelial Progenitor Cells in Periodontitis." Journal of Periodontology 85, no. 12 (December 2014): 1739–47. http://dx.doi.org/10.1902/jop.2014.140153.

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Samman Tahhan, Ayman, Muhammad Hammadah, Heval Mohamed Kelli, Jeong Hwan Kim, Pratik B. Sandesara, Ayman Alkhoder, Belal Kaseer, et al. "Circulating Progenitor Cells and Racial Differences." Circulation Research 123, no. 4 (August 3, 2018): 467–76. http://dx.doi.org/10.1161/circresaha.118.313282.

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Bonsignore, Maria R., Giuseppe Morici, Alessandra Santoro, Maria Pagano, Lucia Cascio, Anna Bonanno, Pietro Abate, et al. "Circulating hematopoietic progenitor cells in runners." Journal of Applied Physiology 93, no. 5 (November 1, 2002): 1691–97. http://dx.doi.org/10.1152/japplphysiol.00376.2002.

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Because endurance exercise causes release of mediators and growth factors active on the bone marrow, we asked whether it might affect circulating hematopoietic progenitor cells (HPCs) in amateur runners [ n = 16, age: 41.8 ± 13.5 (SD) yr, training: 93.8 ± 31.8 km/wk] compared with sedentary controls ( n = 9, age: 39.4 ± 10.2 yr). HPCs, plasma cortisol, interleukin (IL)-6, granulocyte colony-stimulating factor (G-CSF), and the growth factor fms-like tyrosine kinase-3 (flt3)-ligand were measured at rest and after a marathon (M; n = 8) or half-marathon (HM; n = 8). Circulating HPC counts (i.e., CD34+cells and their subpopulations) were three- to fourfold higher in runners than in controls at baseline. They were unaffected by HM or M acutely but decreased the morning postrace. Baseline cortisol, flt3-ligand, IL-6, and G-CSF levels were similar in runners and controls. IL-6 and G-CSF increased to higher levels after M compared with HM, whereas cortisol and flt3-ligand increased similarly postrace. Our data suggest that increased HPCs reflect an adaptation response to recurrent, exercise-associated release of neutrophils and stress and inflammatory mediators, indicating modulation of bone marrow activity by habitual running.

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Hoeg, Rasmus T., Dean A. Jobe, Krista E. Asp, Steven M. Callister, Lori A. Meyer, Michelle A. Mathiason, Craig E. Cole, Wayne A. Bottner, John P. Farnen, and Ronald S. Go. "Circulating Endothelial Cells and Circulating Endothelial Progenitor Cells in Polycythemia Vera." Blood 108, no. 11 (November 16, 2006): 4900. http://dx.doi.org/10.1182/blood.v108.11.4900.4900.

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Abstract Background: Angiogenesis and thrombosis, two conditions associated with perturbation of the vascular endothelium and increased CECs, are frequently observed in PV. We performed this study to quantify and characterize CECs in patients with PV and to determine whether CEC profile is associated with thrombotic complications. We also quantified CEPs in a subgroup of patients. Methods: We used flow cytometry to prospectively analyze CECs and CEPs in the whole blood of healthy patients (n=20) and patients with PV (n=30; 13 treated with hydroxyurea, 12 undergoing phlebotomy alone, and 5 never treated). CECs (CD45−/CD31+/CD146+) were quantified and characterized to determine their apoptotic (annexin stain) or activation (CD106+) states. Cells with CD45−/CD31+/CD133+/VEGF-R2+ immunophenotype were considered CEPs. Results: CEC levels in PV patients were higher compared to healthy controls (median 53 cells/mL [range, 11–392] vs 18.5 cells/mL [range, 4–66]; P< .0001). However, the proportions of apoptotic (17.3% [range, 0–87.5] vs 25.9% [range, 0–57.1]; P= .87) and activated (0.7% [range, 0–28.6] vs 0% [range, 0–57.1]; P= .14) CECs were similar between the two groups. In PV patients with high levels (≥2 SD above control mean or ≥53 cells/mL) of CECs (n=14), 5 (36%) developed thromboses. Four (25%) of 16 PV patients with CEC levels similar to healthy controls developed thromboses. The rates of thrombosis between the groups were not statistically different (P= .69). In addition, CEC count, activation, and apoptosis were similar between the hydroxyurea-treated group and the group not treated with hydroxyurea. We detected low numbers of CEPs in PV patients (n=25) that were similar to controls (4 cells/mL [range, 0–100] vs 8 cells/mL [range, 0–60]; P= .34). Conclusions: CECs, but not CEPs, are significantly increased in PV patients. However, there appears to be no association between CEC number, activation or apoptotic state and the development of thromboses. In addition, hydroxyurea therapy does not appear to effect endothelial cells.

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Richman, CM, and GD Johnson. "Granulocyte/macrophage progenitor cells from peripheral blood and bone marrow differ in their response to prostaglandin E1." Blood 70, no. 6 (December 1, 1987): 1792–96. http://dx.doi.org/10.1182/blood.v70.6.1792.bloodjournal7061792.

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Prostaglandins of the E series (PGE) inhibit proliferation of normal bone marrow granulocyte/macrophage progenitors (CFU-GM). Circulating CFU-GM are known to differ from marrow CFU-GM in many characteristics, and in the present study, we compared the effect of PGE1 on circulating and bone marrow progenitors in normals and in patients with chronic myelogenous leukemia (CML). PGE1 caused a dose-dependent inhibition of normal marrow CFU-GM. Circulating CFU-GM were inhibited only at concentrations of 10(-5) mol/L or greater, and progenitor proliferation was, in fact, significantly stimulated at PGE1 concentrations between 10(-8) and 10(-6) mol/L. Bone marrow CFU-GM from patients with CML were inhibited in a manner similar to that of normal bone marrow. Circulating cells from patients with CML were, however, less sensitive to PGE1 inhibition than CML bone marrow cells and demonstrated a pattern intermediate between normal circulating and normal marrow progenitors. These studies suggest that peripheral blood and bone marrow contain different progenitor cell populations.

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Bilko, N. M., I. S. Dyagil, I. S. Russu, and D. I. Bilko. "CIRCULATING HEMATOPOIETIC PROGENITOR CELLS IN PATIENTS AFFECTED BY CHORNOBYL ACCIDENT." Experimental Oncology 38, no. 4 (December 22, 2016): 242–44. http://dx.doi.org/10.31768/2312-8852.2016.38(4):242-244.

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High radiation sensitivity of stem cells and their ability to accumulate sublethal radiation damage provides the basis for investigation of hematopoietic progenitors using in vivo culture methodology. Unique samples of peripheral blood and bone marrow were derived from the patients affected by Chornobyl accident during liquidation campaign. Aim: To investigate functional activity of circulating hematopoietic progenitor cells from peripheral blood and bone marrow of cleanup workers in early and remote periods after the accident at Chornobyl nuclear power plant (CNPP). Materials and Methods: The assessment of the functional activity of circulating hematopoietic progenitor cells was performed in samples of peripheral blood and bone marrow of 46 cleanup workers, who were treated in the National Scientific Center for Radiation Medicine of the Academy of Medical Sciences of Ukraine alongside with 35 non radiated patients, who served as a control. Work was performed by culturing peripheral blood and bone marrow mononuclear cells in the original gel diffusion capsules, implanted into the peritoneal cavity of CBA mice. Results: It was shown that hematopoietic progenitor cells could be identified in the peripheral blood of liquidators of CNPP accident. At the same time the number of functionally active progenitor cells of the bone marrow was significantly decreased and during the next 10 years after the accident, counts of circulating progenitor cells in the peripheral blood as well as functionally active hematopoietic cells in bone marrow returned to normal levels. Conclusion: It was shown that hematopoietic progenitor cells are detected not only in the bone marrow but also in the peripheral blood of liquidators as a consequence of radiation exposure associated with CNPP accident. This article is a part of a Special Issue entitled “The Chornobyl Nuclear Accident: Thirty Years After”.

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Fadini, Gian Paolo, Mattia Albiero, Lisa Menegazzo, Elisa Boscaro, Carlo Agostini, Saula Vigili de Kreutzenberg, Marcello Rattazzi, and Angelo Avogaro. "Procalcific Phenotypic Drift of Circulating Progenitor Cells in Type 2 Diabetes with Coronary Artery Disease." Experimental Diabetes Research 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/921685.

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Diabetes mellitus (DM) alters circulating progenitor cells relevant for the pathophysiology of coronary artery disease (CAD). While endothelial progenitor cells (EPCs) are reduced, there is no data on procalcific polarization of circulating progenitors, which may contribute to vascular calcification in these patients. In a cohort of 107 subjects with and without DM and CAD, we analyzed the pro-calcific versus endothelial differentiation status of circulating CD34+ progenitor cells. Endothelial commitment was determined by expression of VEGFR-2 (KDR) and pro-calcific polarization by expression of osteocalcin (OC) and bone alkaline phosphatase (BAP). We found that DM patients had significantly higher expression of OC and BAP on circulating CD34+ cells than control subjects, especially in the presence of CAD. In patients with DM and CAD, the ratio of OC/KDR, BAP/KDR, and OC+BAP/KDR was about 3-fold increased than in other groups. EPCs cultured from DM patients with CAD occasionally formed structures highly suggestive of calcified nodules, and the expression of osteogenic markers by EPCs from control subjects was significantly increased in response to the toll-like receptor agonist LPS. In conclusion, circulating progenitor cells of diabetic patients show a phenotypic drift toward a pro-calcific phenotype that may be driven by inflammatory signals.

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Andrews, RG, RA Briddell, GH Knitter, T. Opie, M. Bronsden, D. Myerson, FR Appelbaum, and IK McNiece. "In vivo synergy between recombinant human stem cell factor and recombinant human granulocyte colony-stimulating factor in baboons enhanced circulation of progenitor cells." Blood 84, no. 3 (August 1, 1994): 800–810. http://dx.doi.org/10.1182/blood.v84.3.800.bloodjournal843800.

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Recombinant human stem cell factor (rhSCF) and recombinant human granulocyte colony-stimulating factor (rhG-CSF) are synergistic in vitro in stimulating the proliferation of hematopoietic progenitor cells and their precursors. We examined the in vivo synergy of rhSCF with rhG-CSF for stimulating hematopoiesis in vivo in baboons. Administration of low-dose (LD) rhSCF (25 micrograms/kg) alone did not stimulate changes in circulating WBCs. In comparison, administration of LD rhSCF in combination with rhG-CSF at 10 micrograms/kg or 100 micrograms/kg stimulated increases in circulating WBCs of multiple types up to twofold higher than was stimulated by administration of the same dose of rhG-CSF alone. When the dose of rhG-CSF is increased to 250 micrograms/kg, the administration of LD rhSCF does not further increase the circulating WBC counts. Administration of LD rhSCF in combination with rhG-CSF also stimulated increased circulation of hematopoietic progenitors. LD rhSCF alone stimulated less of an increase in circulating progenitors, per milliliter of blood, than did administration of rhG-CSF alone at 100 micrograms/kg. Baboons administered LD rhSCF together with rhG-CSF at 10, 100, or 250 micrograms/kg had 3.5- to 16-fold higher numbers per milliliter of blood of progenitors cells of multiple types, including colony-forming units granulocyte/macrophage (CFU-GM), burst-forming unit-erythroid (BFU-E), and colony-forming and burst-forming units-megakaryocyte (CFU- MK and BFU-MK) compared with animals given the same dose of rhG-CSF without rhSCF, regardless of the rhG-CSF dose. The increased circulation of progenitor cells stimulated by the combination of rhSCF plus rhG-CSF was not necessarily directly related to the increase in WBCs, as this effect on peripheral blood progenitors was observed even at an rhG-CSF dose of 250 micrograms/kg, where coadministration of LD rhSCF did not further increase WBC counts. Administration of very-low- dose rhSCF (2.5 micrograms/kg) with rhG-CSF, 10 micrograms/kg, did not stimulate increases in circulating WBCs, but did increase the number of megakaryocyte progenitor cells in blood compared with rhG-CSF alone. LD rhSCF administered alone for 7 days before rhG-CSF did not result in increased levels of circulating WBCs or progenitors compared with rhG- CSF alone. Thus, the synergistic effects of rhSCF with rhG-CSF were both dose- and time-dependent. The doses of rhSCF used in these studies have been tolerated in vivo in humans.(ABSTRACT TRUNCATED AT 400 WORDS).

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Richman, CM, and GD Johnson. "Granulocyte/macrophage progenitor cells from peripheral blood and bone marrow differ in their response to prostaglandin E1." Blood 70, no. 6 (December 1, 1987): 1792–96. http://dx.doi.org/10.1182/blood.v70.6.1792.1792.

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Abstract Prostaglandins of the E series (PGE) inhibit proliferation of normal bone marrow granulocyte/macrophage progenitors (CFU-GM). Circulating CFU-GM are known to differ from marrow CFU-GM in many characteristics, and in the present study, we compared the effect of PGE1 on circulating and bone marrow progenitors in normals and in patients with chronic myelogenous leukemia (CML). PGE1 caused a dose-dependent inhibition of normal marrow CFU-GM. Circulating CFU-GM were inhibited only at concentrations of 10(-5) mol/L or greater, and progenitor proliferation was, in fact, significantly stimulated at PGE1 concentrations between 10(-8) and 10(-6) mol/L. Bone marrow CFU-GM from patients with CML were inhibited in a manner similar to that of normal bone marrow. Circulating cells from patients with CML were, however, less sensitive to PGE1 inhibition than CML bone marrow cells and demonstrated a pattern intermediate between normal circulating and normal marrow progenitors. These studies suggest that peripheral blood and bone marrow contain different progenitor cell populations.

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Fadini, Gian Paolo, Mattia Albiero, Andrea Cignarella, Chiara Bolego, Christian Pinna, Elisa Boscaro, Elisa Pagnin, et al. "Effects of androgens on endothelial progenitor cells in vitro and in vivo." Clinical Science 117, no. 10 (September 7, 2009): 355–64. http://dx.doi.org/10.1042/cs20090077.

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The beneficial or detrimental effects of androgens on the cardiovascular system are debated. Endothelial progenitor cells are bone-marrow-derived cells involved in endothelial healing and angiogenesis, which promote cardiovascular health. Oestrogens are potent stimulators of endothelial progenitor cells, and previous findings have indicated that androgens may improve the biology of these cells as well. In the present study, we show that testosterone and its active metabolite dihydrotestosterone exert no effects on the expansion and function of late endothelial progenitors isolated from the peripheral blood of healthy human adult males, whereas they positively modulate early ‘monocytic’ endothelial progenitor cells. In parallel, we show that castration in rats is followed by a decrease in circulating endothelial progenitor cells, but that testosterone and dihydrotestosterone replacement fails to restore endothelial progenitor cells towards normal levels. This is associated with persistently low oestrogen levels after androgen replacement in castrated rats. In a sample of 62 healthy middle-aged men, we show that circulating endothelial progenitor cell levels are more directly associated with oestradiol, rather than with testosterone, concentrations. In conclusion, our results collectively demonstrate that androgens exert no direct effects on endothelial progenitor cell biology in vitro and in vivo.

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Zahran, Asmaa M., Ismail L. Mohamed, Osama M. El Asheer, Deiaaeldin M. Tamer, Mohamed G. M. Abo-ELela, Mona H. Abdel-Rahim, Omnia H. B. El-Badawy, and Khalid I. Elsayh. "Circulating Endothelial Cells, Circulating Endothelial Progenitor Cells, and Circulating Microparticles in Type 1 Diabetes Mellitus." Clinical and Applied Thrombosis/Hemostasis 25 (January 1, 2019): 107602961882531. http://dx.doi.org/10.1177/1076029618825311.

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Background and Aim: Hyperglycemia in type 1 diabetes (T1D) is accompanied by endothelial cell dysfunction which is known to contribute to the pathogenesis of cardiovascular disorders. The aim of the current study was to explore the profile of circulating endothelial progenitor cells (EPCs), circulating endothelial cells (CECs), endothelial and platelet derived micropaticles (EMPs, PMPs) and total microparticles (TMPs), in T1D children in relation to each other and to the metabolic disorders accompanying T1D. Patients and Methods: Thirty T1D patients and 20 age and sex matched healthy volunteers were assessed for HbA1c level and lipid profile. Quantification of CECs, EPCs, TMPs, EMPs and PMPs was done by flow cytometry. Results: The mean levels of EMPs, PMPs, TMPs and CECs were significantly higher in diabetic children compared to controls. Meanwhile, the levels of EPCs were significantly lower in diabetic children compared to controls. Both PMPs and CECs showed the highest significant differences between patients and controls and their levels were directly related to HbA1c, total cholesterol, LDL and triglycerides. A moderate correlation was observed between the frequency of PMPs and CECs. EPCs revealed negative correlations with both LDL and triglycerides. TMPs were only related to LDL, while EMPs were only related to HbA1c. Conclusion: Although there is disturbance in the levels of EMPs, PMPs, TMPs, CECs and EPCs in type 1 diabetic children compared to the controls, only the levels of PMPs and CECs were closely affected by the poor glycemic control and dyslipidemia occurring in T1D; thus may contribute to a higher risk of cardiovascular diseases.

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Rafat, Neysan, Grietje Ch Beck, Jutta Schulte, Jochen Tuettenberg, and Peter Vajkoczy. "Circulating endothelial progenitor cells in malignant gliomas." Journal of Neurosurgery 112, no. 1 (January 2010): 43–49. http://dx.doi.org/10.3171/2009.5.jns081074.

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Object Recent experimental work suggests that circulating endothelial progenitor cells (cEPCs) are recruited to the angiogenic vascular system of malignant gliomas. Consequently, the level of cEPCs has been proposed as a novel biomarker for the diagnosis and monitoring of these lesions. The aim of the present study was to examine the level of cEPCs and the level of EPC mobilizing mediators in the blood of patients with malignant gliomas. The authors were also interested in whether a correlation could be observed between the level of cEPCs and the extent of glioma angiogenesis determined by conventional methods. Methods Peripheral blood mononuclear cells from the whole blood of 12 patients with malignant gliomas (all glioblastomas multiforme [GBMs]), 10 with metastases to the brain, and 10 healthy volunteers were isolated using Ficoll density gradient centrifugation. The number of cEPCs was quantified by fluorescence-activated cell sorting analysis using antibodies against CD34, CD133, and VEGFR-2. Serum concentrations of VEGF and granulocyte-macrophage colony-stimulating factor (GM-CSF) were determined using the enzyme-linked immunosorbent assay. Histological analysis of tumor blood vessel density was performed by CD34 immunohistochemical staining. Results The number of cEPCs was significantly higher in patients with GBMs than in those with metastases (p < 0.04) or in the healthy volunteers (p < 0.004). The serum VEGF concentrations in patients with GBMs and metastases were significantly higher than in the healthy volunteers (p < 0.0001). Similar findings were observed for concentrations of GM-CSF. In addition, the patients in the GBM group with higher levels of cEPCs had significantly higher tumor blood vessel densities (1.71 ± 1.17% of total area) compared with patients who had low levels of cEPCs (0.62 ± 0.28% of total area; p < 0.02). Conclusions Endothelial progenitor cells are increasingly mobilized in patients with malignant gliomas, and their levels correlate with tumor angiogenic activity. Therefore, the authors' results suggest that cEPCs may have the potential to serve as a novel biomarker for the identification of patients who would benefit from antiangiogenic therapy for GBM.

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Mehrad, Borna, Michael P. Keane, Brigitte N. Gomperts, and Robert M. Strieter. "Circulating progenitor cells in chronic lung disease." Expert Review of Respiratory Medicine 1, no. 1 (August 2007): 157–65. http://dx.doi.org/10.1586/17476348.1.1.157.

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Kang, Hyun-Seung, Kyu-Chang Wang, and Seung-Ki Kim. "Circulating Vascular Progenitor Cells in Moyamoya Disease." Journal of Korean Neurosurgical Society 57, no. 6 (2015): 428. http://dx.doi.org/10.3340/jkns.2015.57.6.428.

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Geft, Dael, Shmuel Schwartzenberg, and Jacob George. "Circulating endothelial progenitor cells in cardiovascular disorders." Expert Review of Cardiovascular Therapy 6, no. 8 (September 2008): 1115–21. http://dx.doi.org/10.1586/14779072.6.8.1115.

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Song, J., Y. Chung, Y. Kim, J. Lee, N. Lee, and H. Bae. "Circulating endothelial progenitor cells in gynecologic cancer." Gynecologic Oncology 130, no. 1 (July 2013): e160-e161. http://dx.doi.org/10.1016/j.ygyno.2013.04.449.

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Moneta, G. L. "Circulating Endothelial Progenitor Cells and Cardiovascular Outcomes." Yearbook of Vascular Surgery 2007 (January 2007): 11–12. http://dx.doi.org/10.1016/s0749-4041(08)70347-6.

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Ural, S. H. "Circulating Endothelial Progenitor Cells During Human Pregnancy." Yearbook of Obstetrics, Gynecology and Women's Health 2006 (January 2006): 21. http://dx.doi.org/10.1016/s1090-798x(08)70309-6.

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Kim, Yoon Byoung, Ye Won Chung, Hyo Sook Bae, Jae Kwan Lee, Nak Woo Lee, Kyu Wan Lee, and Jae Yun Song. "Circulating endothelial progenitor cells in gynaecological cancer." Journal of International Medical Research 41, no. 2 (March 14, 2013): 293–99. http://dx.doi.org/10.1177/0300060513476999.

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Rochefort, G. Y. "Circulating progenitor cells in coronary heart disease." Heart 94, no. 6 (June 1, 2008): 793–94. http://dx.doi.org/10.1136/hrt.2008.141812.

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Werner, N., S. Kosiol, and T. Schiegle. "Circulating Endothelial Progenitor Cells in Cardiovascular Outcomes." Journal of Vascular Surgery 43, no. 1 (January 2006): 196. http://dx.doi.org/10.1016/j.jvs.2005.12.021.

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Christensen, Robert D. "Circulating pluripotent hematopoietic progenitor cells in neonates." Journal of Pediatrics 110, no. 4 (April 1987): 622–25. http://dx.doi.org/10.1016/s0022-3476(87)80564-4.

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Werner, Nikos, Sonja Kosiol, Tobias Schiegl, Patrick Ahlers, Katrin Walenta, Andreas Link, Michael Böhm, and Georg Nickenig. "Circulating Endothelial Progenitor Cells and Cardiovascular Outcomes." New England Journal of Medicine 353, no. 10 (September 8, 2005): 999–1007. http://dx.doi.org/10.1056/nejmoa043814.

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Cimato, Thomas R., Alexis Conway, Julianne Nichols, and Paul K. Wallace. "CD133 expression in circulating hematopoietic progenitor cells." Cytometry Part B: Clinical Cytometry 96, no. 1 (October 16, 2018): 39–45. http://dx.doi.org/10.1002/cyto.b.21732.

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Werner, N., S. Kosiol, and T. Schiegl. "Circulating Endothelial Progenitor Cells and Cardiovascular Outcomes." ACC Current Journal Review 14, no. 12 (December 2005): 3. http://dx.doi.org/10.1016/j.accreview.2005.11.011.

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Kleinman, Mark E., Francine Blei, and Geoffrey C. Gurtner. "Circulating Endothelial Progenitor Cells and Vascular Anomalies." Lymphatic Research and Biology 3, no. 4 (December 2005): 234–39. http://dx.doi.org/10.1089/lrb.2005.3.234.

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Mandraffino, G., C. O. Aragona, S. Quartuccio, V. Cairo, F. Mamone, M. A. Sardo, A. Saitta, and E. Imbalzano. "[PP.31.01] CIRCULATING PROGENITOR CELLS IN HYPERTENSION." Journal of Hypertension 34 (September 2016): e314. http://dx.doi.org/10.1097/01.hjh.0000492258.26533.9e.

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Sugawara, Junichi, Minori Mitsui-Saito, Tetsuro Hoshiai, Chika Hayashi, Yoshitaka Kimura, and Kunihiro Okamura. "Circulating Endothelial Progenitor Cells during Human Pregnancy." Journal of Clinical Endocrinology & Metabolism 90, no. 3 (March 2005): 1845–48. http://dx.doi.org/10.1210/jc.2004-0541.

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Soler, Maria Jose, Ofelia Maria Martinez-Estrada, Josep Maria Puig-Mari, Didac Marco-Feliu, Anna Oliveras, Joan Vila, Marisa Mir, Antonia Orfila, Senen Vilaro, and Josep Lloveras. "Circulating Endothelial Progenitor Cells After Kidney Transplantation." American Journal of Transplantation 5, no. 9 (September 2005): 2154–59. http://dx.doi.org/10.1111/j.1600-6143.2005.01010.x.

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Jung, Keun-Hwa, and Jae-Kyu Roh. "Circulating Endothelial Progenitor Cells in Cerebrovascular Disease." Journal of Clinical Neurology 4, no. 4 (2008): 139. http://dx.doi.org/10.3988/jcn.2008.4.4.139.

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Ravens, U. "Atrial fibrillation and circulating endothelial progenitor cells." Europace 12, no. 4 (February 6, 2010): 460–61. http://dx.doi.org/10.1093/europace/euq010.

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Doerschuk, C. M. "Circulating endothelial progenitor cells in pulmonary inflammation." Thorax 60, no. 5 (May 1, 2005): 362–64. http://dx.doi.org/10.1136/thx.2004.037796.

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Kort, Eric J., Lacey Croskey, Taryn Scibienski, Surender Rajasekaran, and Stefan Jovinge. "Circulating Progenitor Cells and Childhood Cardiovascular Disease." Pediatric Cardiology 37, no. 2 (November 11, 2015): 225–31. http://dx.doi.org/10.1007/s00246-015-1300-8.

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Bulut*, Daniel, Nadine Albrecht*, Matthias Imöhl, Bülent Günesdogan, Nadine Bulut-Streich, Jan Börgel, Christoph Hanefeld, Michael Krieg, and Andreas Mügge. "Hormonal status modulates circulating endothelial progenitor cells." Clinical Research in Cardiology 96, no. 5 (February 26, 2007): 258–63. http://dx.doi.org/10.1007/s00392-007-0494-z.

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Mucciolo, Dario Pasquale, Rossella Marcucci, Andrea Sodi, Francesca Cesari, Vittoria Murro, Angela Rogolino, Stanislao Rizzo, et al. "Circulating endothelial and progenitor cells in age-related macular degeneration." European Journal of Ophthalmology 30, no. 5 (July 22, 2019): 956–65. http://dx.doi.org/10.1177/1120672119863306.

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Purpose: To evaluate circulating endothelial and circulating progenitor cells as biomarkers in age-related macular degeneration patients (both exudative and atrophic forms) in order to establish the possible clinical implication of their assessment. Methods: We have enrolled 44 age-related macular degeneration patients: 22 patients with a recently diagnosed exudative (neovascular) form (Group A) and 22 patients with an atrophic (dry) form (Group B). The control group consisted of 22 age and sex-matched healthy subjects (Group C). The number of circulating endothelial progenitor cells (CD34+/KDR+, CD133+/KDR+, and CD34+/KDR+/CD133+), circulating progenitor cells (CD34+, CD133+, and CD34+/CD133+), and circulating endothelial cells were determined in the peripheral venous blood samples by flow cytometry. Neovascular age-related macular degeneration patients were evaluated at baseline and 4 weeks after a loading phase of three consequent intravitreal injections of ranibizumab. Results: Comparing age-related macular degeneration patients with the control group, endothelial progenitor cell and circulating progenitor cell levels were not significantly different, while age-related macular degeneration patients showed significantly higher levels of circulating endothelial cells ( p = 0.001). Anti–vascular endothelial growth factor treatment with intravitreal ranibizumab was associated with a significant reduction of endothelial progenitor cell levels, with no significant influence on circulating progenitor cells and circulating endothelial cells. Conclusion: We reported higher levels of circulating endothelial cells in age-related macular degeneration patients in comparison with the control group, thereby supporting the hypothesis of an involvement of endothelial dysregulation in the age-related macular degeneration and a reduction of the endothelial progenitor cell level in neovascular age-related macular degeneration patients after three intravitreal injections of ranibizumab.

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Woywodt, Alexander, Francesco Bertolini, Todd Bull, Jill Buyon, Robert Clancy, Marion Haubitz, Robert Hebbel, et al. "Circulating endothelial cells." Thrombosis and Haemostasis 93, no. 02 (2005): 228–35. http://dx.doi.org/10.1160/th04-09-0578.

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SummaryRecent research has recognised new populations of non-hematopoïetic cells in the blood. One of these, circulating endothelial cells (CECs), often defined by the expression of membrane glycoprotein CD146, are rarely found in the blood in health, but raised numbers are present in a wide variety of human conditions, including inflammatory, immune, infectious, neoplastic and cardiovascular disease, and seem likely to be evidence of profound vascular insult. An additional population are endothelial progenitor cells, defined by the co-expression of endothelial and immaturity cell surface molecules and also by the ability to form colonies in vitro. Although increased numbers of CECs correlate with other markers of vascular disease, questions remain regarding the precise definition, cell biology and origin of CECs. For example, they may be damaged, necrotic or apopototic, or alive, and could possess procoagulant and/or proinflammatory properties. However, since these cells seem to be representative of in situ endothelium, their phenotype may provide useful information. Indeed, whatever their phenotype, there is growing evidence that CECs may well be a novel biomarker, the measurement of which will have utility in various clinical settings related to vascular injury. Despite this promise, progress is impeded by the diversity of methodologies used to detect these cells. Accordingly, results are sometimes inconclusive and even conflicting. Nevertheless, increased CECs predict adverse cardiovascular events in acute coronary syndromes, suggesting they may move from being simply a research index to having a role in the clinic. The objective of the present communication is to condense existing data on CECs, briefly compare them with progenitor cells, and summarise possible mechanism(s) by which they may contribute to vascular pathology.

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Campagnoli, Cesare, Nicholas Fisk, Timothy Overton, Phillip Bennett, Timothy Watts, and Irene Roberts. "Circulating hematopoietic progenitor cells in first trimester fetal blood." Blood 95, no. 6 (March 15, 2000): 1967–72. http://dx.doi.org/10.1182/blood.v95.6.1967.

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Abstract The yolk sac and aorto-gonad-mesonephros region are well recognized as the principal sites of hematopoiesis in the developing embryo, and the liver is the principal site of hematopoiesis in the fetus. However, little is known about circulating hematopoietic stem and progenitor cells in early fetal life. We investigated the number and characteristics of circulating progenitors in first trimester blood of 64 human fetuses (median gestational age, 10+4 weeks; range, 7+6-13+6 weeks). CD34+ cells accounted for 5.1 ± 1.0% of CD45+ cells in first trimester blood, which is significantly more than in term cord blood (0.4 ± 0.03%;P = .0015). However, the concentration of CD34+ cells (6.6 ± 2.4 × 104/mL) was similar to that in term cord blood (5.6 ± 3.9 × 104/mL). The total number of progenitors cultured from unsorted mononuclear cells (MNCs) in first trimester blood was 19.2 ± 2.1 × 103/mL, which is similar to that in term cord blood (26.4 ± 5.6 × 103/mL). All lineages were seen: colony-forming unit–GEMM (CFU-GEMM), CFU-GM, BFU-e, BFU-MK, and CFU-MK. Clonogenic assays of CD34+ cells purified from first trimester samples produced mainly two lineages: BFU-e (39.0 ± 9.6 × 103/mL CD34+ cells) and CFU-GEMM (22.6 ± 4.7 × 103/mL CD34+ cells). Short-term liquid culture of first trimester blood MNCs in SCF + IL-3 + Flt-3 (stem cell factor + interleukin-3 + Flt-3) increased, by 7-fold, the numbers of CFU-GEMM and induced a dramatic increase in BFU-e (65.6 ± 12.1–fold). These data show that significant numbers of committed and multipotent progenitors with capacity for expansion circulate in first trimester fetal blood and can be CD34 selected. These cells should be suitable targets for gene transfer and stem cell transplantation and, because fetal hematopoietic progenitors have been demonstrated in the maternal circulation from early gestation, may also be manipulated for noninvasive prenatal diagnosis of major genetic disorders.

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Scheding, S., JE Media, MA KuKuruga, and A. Nakeff. "In situ radiation sensitivity of recombinant human granulocyte colony- stimulating factor-recruited murine circulating blood and bone marrow progenitors (colony-forming unit [CFU]-granulocyte-macrophage and CFU- megakaryocyte): evidence for possible biologic differences between mobilized blood and bone marrow." Blood 88, no. 2 (July 15, 1996): 472–78. http://dx.doi.org/10.1182/blood.v88.2.472.bloodjournal882472.

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Increasing evidence especially stemming from peripheral blood progenitor transplantation studies points to a possible biologic difference between mobilized blood and bone marrow progenitor cells. The objective of this study was to compare the in situ radiation sensitivity of recombinant human granulocyte colony-stimulating factor (rhG-CSF)-recruited circulating granulopoietic (blood colony-forming unit-granulocyte-macrophage [CFU-GM(blood)]) and megakaryocytopoietic (blood CFU-megakaryocyte [CFU-Meg(blood)]) progenitors, with the nonmobilized fraction remaining in the bone marrow (CFU-GM(femur) and CFU-Meg(femur)). Splenectomized male B6D2F1 mice received 50 micrograms/kg/d rhG-CSF daily for 8 days to induce high levels of circulating progenitors, followed by either total body X-irradiation (TBI) or X-irradiation of the chest (CI) with 62.5, 125, 250, or 500 cGy. Progenitor cells were assayed 24 hours after irradiation. Circulating CFU-GM and CFU-Meg in the blood were decreased in a dose- dependent fashion by both TBI and CI, with TBI causing greater damage than CI. Average D0 values for TBI were 53 cGy for CFU-GM(blood) and 40 cGy for CFU-Meg(blood) D0 values for CI were 90 cGy for CFU-GM(blood) and 140 cGy for CFU-Meg(blood). As seen for blood progenitor cells, TBI caused a dose-dependent decrease of both CFU-GM(femur) (D0, 136 cGy) and CFU-Meg(femur) (D0, 148 cGy). However, radiation-induced bone marrow progenitor cell kill was significantly lower when compared with blood progenitors. Despite the fact that circulating blood elements only received a fraction of the total dose administered as Cl, the extent of blood progenitor kill caused by Cl was higher than the effects of identical TBI doses on bone marrow CFU. The results of this study showed that rhG-CSF-recruited CFU-Meg(blood) and CFU-GM(blood) were considerably more radiosensitive than femoral progenitors, thereby providing novel evidence for a biologic difference between rhG-CSF- recruited peripheral blood progenitors and the nonrecruited bone marrow CFU.

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Andrews, RG, RA Briddell, GH Knitter, T. Opie, M. Bronsden, D. Myerson, FR Appelbaum, and IK McNiece. "In vivo synergy between recombinant human stem cell factor and recombinant human granulocyte colony-stimulating factor in baboons enhanced circulation of progenitor cells." Blood 84, no. 3 (August 1, 1994): 800–810. http://dx.doi.org/10.1182/blood.v84.3.800.800.

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Abstract Recombinant human stem cell factor (rhSCF) and recombinant human granulocyte colony-stimulating factor (rhG-CSF) are synergistic in vitro in stimulating the proliferation of hematopoietic progenitor cells and their precursors. We examined the in vivo synergy of rhSCF with rhG-CSF for stimulating hematopoiesis in vivo in baboons. Administration of low-dose (LD) rhSCF (25 micrograms/kg) alone did not stimulate changes in circulating WBCs. In comparison, administration of LD rhSCF in combination with rhG-CSF at 10 micrograms/kg or 100 micrograms/kg stimulated increases in circulating WBCs of multiple types up to twofold higher than was stimulated by administration of the same dose of rhG-CSF alone. When the dose of rhG-CSF is increased to 250 micrograms/kg, the administration of LD rhSCF does not further increase the circulating WBC counts. Administration of LD rhSCF in combination with rhG-CSF also stimulated increased circulation of hematopoietic progenitors. LD rhSCF alone stimulated less of an increase in circulating progenitors, per milliliter of blood, than did administration of rhG-CSF alone at 100 micrograms/kg. Baboons administered LD rhSCF together with rhG-CSF at 10, 100, or 250 micrograms/kg had 3.5- to 16-fold higher numbers per milliliter of blood of progenitors cells of multiple types, including colony-forming units granulocyte/macrophage (CFU-GM), burst-forming unit-erythroid (BFU-E), and colony-forming and burst-forming units-megakaryocyte (CFU- MK and BFU-MK) compared with animals given the same dose of rhG-CSF without rhSCF, regardless of the rhG-CSF dose. The increased circulation of progenitor cells stimulated by the combination of rhSCF plus rhG-CSF was not necessarily directly related to the increase in WBCs, as this effect on peripheral blood progenitors was observed even at an rhG-CSF dose of 250 micrograms/kg, where coadministration of LD rhSCF did not further increase WBC counts. Administration of very-low- dose rhSCF (2.5 micrograms/kg) with rhG-CSF, 10 micrograms/kg, did not stimulate increases in circulating WBCs, but did increase the number of megakaryocyte progenitor cells in blood compared with rhG-CSF alone. LD rhSCF administered alone for 7 days before rhG-CSF did not result in increased levels of circulating WBCs or progenitors compared with rhG- CSF alone. Thus, the synergistic effects of rhSCF with rhG-CSF were both dose- and time-dependent. The doses of rhSCF used in these studies have been tolerated in vivo in humans.(ABSTRACT TRUNCATED AT 400 WORDS).

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Lord, BI, LB Woolford, LM Wood, LG Czaplewski, M. McCourt, MG Hunter, and RM Edwards. "Mobilization of early hematopoietic progenitor cells with BB-10010: a genetically engineered variant of human macrophage inflammatory protein- 1 alpha." Blood 85, no. 12 (June 15, 1995): 3412–15. http://dx.doi.org/10.1182/blood.v85.12.3412.bloodjournal85123412.

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BB-10010 is a genetically engineered variant of human macrophage inflammatory protein-1 alpha with improved solution properties. We show here that it mobilizes stem cells into the peripheral blood. We investigated the mobilizing effects of BB-10010 on the numbers of circulating 8-day spleen colony-forming units (CFU-S8), CFU-S12, and progenitors with marrow repopulating ability (MRA). A single subcutaneous dose of BB-10010 caused a twofold increase in circulating numbers of CFU-S8, CFU-S12, and MRA 30 minutes after dosing. We also investigated the effects of granulocyte colony-stimulating factor (G-CSF) and the combination of G-CSF with BB-10010 on progenitor mobilization. Two days of G-CSF treatment increased circulating CFU-S8, CFU-S12, and MRA progenitors by 25.7-, 19.8-, and 27.7-fold. A single administration of BB-10010 after 2 days of G-CSF treatment increased circulating CFU-S8, CFU-S12, and MRA even further to 38-, 33-, and 100-fold. Splenectomy resulted in increased circulating progenitor numbers but did not change the pattern of mobilization. Two days of treatment with G-CSF then increased circulating CFU-S8, CFU-S12, and MRA by 64-, 69-, and 32-fold. A single BB-10010 administration after G-CSF treatment further increased them to 85-, 117-, and 140-fold, respectively, compared with control. We conclude that BB-10010 causes a rapid increase in the number of circulating hematopoietic progenitors and further enhances the numbers induced by pretreatment with G-CSF. BB-10010 preferentially mobilized the more primitive progenitors with marrow repopulating activity, releasing four times the number achieved with G-CSF alone. Translated into a clinical setting, this improvement in progenitor cell mobilization may enhance the efficiency of harvest and the quality of grafts for peripheral blood stem cell transplantation.

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Shimoni, Sara, Iris Bar, Liaz Zilberman, Sorel Goland, Orly Edri, Gera Gandelman, Arnon Afek, Ari Shamiss, and Jacob George. "Circulating Progenitor and Apoptotic Progenitor Cells in Patients With Aortic Regurgitation." Circulation Journal 77, no. 3 (2013): 764–71. http://dx.doi.org/10.1253/circj.cj-12-0694.

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Bulduk, T., A. U. Yalcin, O. M. Akay, S. G. Ozkurt, H. U. Teke, G. Sahin, G. Temiz, and G. Demirel. "Does erythropoietin therapy affect circulating endothelial cells in hemodialysis patients?" Ukrainian Journal of Nephrology and Dialysis, no. 4(68) (October 16, 2020): 29–37. http://dx.doi.org/10.31450/ukrjnd.4(68).2020.05.

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Anemia is a common complication of chronic kidney disease (CKD). The most common cause of anemia in CKD is erythropoietin deficiency; and the most important cause of mortality in CKD patients is atherosclerotic vascular complications which are associated with endothelial damage. One of the methods evaluating vascular integrity is the cytometric measurement of circulating endothelial cells and endothelial progenitor cells in peripheral blood. The study aimed to investigate the effects of erythropoietin therapy on endothelial dysfunction by evaluating circulating endothelial cells and endothelial progenitor cells in peripheral blood using the technique of flow cytometry. Methods. A total of 55 hemodialysis patients were evaluated in three groups; those having erythropoietin therapy for at least last 3 months (n = 20) / not having erythropoietin for at least the last 3 months (n = 20) and the patients who started erythropoietin treatment during the study (n = 5). The control group consisted of 20 people. Blood values of the 3rd Group were investigated three times as baseline, 2nd week and 8th week CD34 +, CD105 + cells were evaluated as activated circulating endothelial cells; CD133 +, CD146 + cells were evaluated as activated endothelial progenitor cells. Results. There was no difference between the patients and healthy individuals in terms of circulating endothelial cells and endothelial progenitor cells. In the third group, no differences were observed in circulating endothelial cells / endothelial progenitor cell levels at baseline / 2nd and 8th weeks. There was no correlation between erythropoietin and circulating endothelial cells / endothelial progenitor cells. Conclusion. A correlation is not available between the therapeutic doses of erythropoietin used in hemodialysis patients and circulating endothelial cells / endothelial progenitor cell levels; supratherapeutic doses could change the results.

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Kolonin, Mikhail, Yan Zhang, Paul J. Simmons, and Charles Bellows. "Circulating Mesenchymal Stromal Cells As a New Prospective Cancer Marker,." Blood 118, no. 21 (November 18, 2011): 3404. http://dx.doi.org/10.1182/blood.v118.21.3404.3404.

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Abstract Abstract 3404 Mobilization of progenitor cells is implicated in pathology and can be indicative of disease progression. Recently, we reported the influence of body mass index (BMI) on level of circulating progenitor cells (Bellows et al., Obesity 2011). Comparative analysis of peripheral blood mononuclear cells (PBMC) from 12 non-obese (BMI < 30) and 14 obese (BMI > 30) disease-free donors by flow cytometry revealed that obesity is associated with a 10-fold increased frequency of circulating mesenchymal stromal progenitor cells (MSC), which circulate at a very low level in healthy lean individuals. We showed that obesity is also associated with a 5-fold increased frequency of circulating progenitor cells (CPC), a population consisting of hematopoietic and endothelial precursors, while the frequencies of mature endothelial cells (EC) and CD34-bright leukocytes (CD34b LC) are unaffected by BMI. Here, we followed up on the assessment of circulating MSC as a potential surrogate pathology marker by analyzing the frequency of circulating CD34-positive progenitor and endothelial cells in a cohort of colorectal cancer patients. PBMC were collected from 45 obese and lean cancer patients and compared to control cancer-free donors. Flow cytometric enumeration of cells was performed based on established immunophenotypes: CD34brightCD31dimCD45dim (CPC), CD34dimCD31brightCD45- (EC), CD34brightCD31-CD45- (MSC) and CD34brightCD45bright CD34b (LC). Groups were compared using multivariate regression analysis. After adjusting for co-founders such as age and BMI, the mean frequencies of MSC and CD34bLC, but not of CPC and EC, were found to be significantly higher in the circulation of CRC patients compared to cancer-free donors. Interestingly, the frequency of circulating MSC, but not of the other cell populations, was also found to be significantly higher in the circulation of obese CRC patients compared to lean CRC patients and obese cancer-free controls. We conclude that markedly increased frequency of MSC in the peripheral blood may represent a new diagnostic CRC marker. BMI-dependent changes in circulating MSC, potentially mobilized from adipose tissue may reveal their trafficking to tumors, which could be one of the mechanistic links between obesity and cancer progression. Validation of MSC as a new surrogate marker of cancer could provide a tool for determining prognosis, predicting response to therapy, and detecting relapse following treatment. Disclosures: No relevant conflicts of interest to declare.

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Journal articles on the topic 'Circulating progenitor cells'

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