scholarly journals Angiogenesis and vasculogenesis: Inducing the growth of new blood vessels and wound healing by stimulation of bone marrow–derived progenitor cell mobilization and homing

2007 ◽  
Vol 45 (6) ◽  
pp. A39-A47 ◽  
Author(s):  
Omaida C. Velazquez
Keyword(s):  
Bone Marrow ◽  
Wound Healing ◽  
Blood Vessels ◽  
Progenitor Cell ◽  
Cell Mobilization ◽  
Stimulation Of

scholarly journals Heparanase regulates retention and proliferation of primitive Sca-1+/c-Kit+/Lin− cells via modulation of the bone marrow microenvironment

Blood ◽  
2008 ◽  
Vol 111 (10) ◽  
pp. 4934-4943 ◽  
Author(s):  
Asaf Spiegel ◽  
Eyal Zcharia ◽  
Yaron Vagima ◽  
Tomer Itkin ◽  
Alexander Kalinkovich ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Cathepsin K ◽  
Hematopoietic Progenitors ◽  
Hematopoietic Progenitor ◽  
Cell Mobilization ◽  
Tumor Growth And Metastasis

Abstract Heparanase is involved in tumor growth and metastasis. Because of its unique cleavage of heparan sulfate, which binds cytokines, chemokines and proteases, we hypothesized that heparanase is also involved in regulation of early stages of hematopoiesis. We report reduced numbers of maturing leukocytes but elevated levels of undifferentiated Sca-1+/c-Kit+/Lin− cells in the bone marrow (BM) of mice overexpressing heparanase (hpa-Tg). This resulted from increased proliferation and retention of the primitive cells in the BM microenvironment, manifested in increased SDF-1 turnover. Furthermore, heparanase overexpression in mice was accompanied by reduced protease activity of MMP-9, elastase, and cathepsin K, which regulate stem and progenitor cell mobilization. Moreover, increased retention of the progenitor cells also resulted from up-regulated levels of stem cell factor (SCF) in the BM, in particular in the stem cell–rich endosteum and endothelial regions. Increased SCF-induced adhesion of primitive Sca-1+/c-Kit+/Lin− cells to osteoblasts was also the result of elevation of the receptor c-Kit. Regulation of these phenomena is mediated by hyperphosphorylation of c-Myc in hematopoietic progenitors of hpa-Tg mice or after exogenous heparanase addition to wildtype BM cells in vitro. Altogether, our data suggest that heparanase modification of the BM microenvironment regulates the retention and proliferation of hematopoietic progenitor cells.

scholarly journals The bone marrow-derived endothelial progenitor cell response is impaired in delayed wound healing from ischemia

2006 ◽  
Vol 43 (1) ◽  
pp. 134-141 ◽  
Author(s):  
Stephen M. Bauer ◽  
Lee J. Goldstein ◽  
Richard J. Bauer ◽  
Haiying Chen ◽  
Mary Putt ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Wound Healing ◽  
Endothelial Progenitor Cell ◽  
Cell Response ◽  
Progenitor Cell ◽  
Endothelial Progenitor ◽  
Delayed Wound Healing

Modulating Cholesterol Levels on Bone Marrow Cells Affects Endothelial and Hematopoietic Cell Mobilization and Differentiation.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1413-1413
Author(s):  
Ana Gomes ◽  
Rita Fragoso ◽  
Catia Igreja ◽  
Sergio Dias
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Progenitor Cells ◽  
B Lymphocytes ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Myeloid Cells ◽  
Hematopoietic Cell ◽  
Hematopoietic Differentiation ◽  
Cell Mobilization

Abstract A decrease in cholesterol (CH) levels associated with hematological malignancies, such as acute leukemia, correlates with Hematopoietic suppression. Moreover, patients with mevalonate kinase deficiency (which results in hypocholesterolemia) have besides neurological defects, hepatosplenomegaly, thrombocytopenia, anemia and eventually progress into Myelodisplasic Syndromes/Leukemia. For this study, we hypothesized that CH levels might affect hematopoietic differentiation (acting directly on hematopoietic stem cells, HSC) or hematopoietic cell mobilization. For this purpose we started by studying the bone marrow (BM) expression pattern of CD36 and ApoE, 2 proteins involved in CH cellular transport, in BM samples of normal adult mice. Immunofluorescent staining showed that CD36 and ApoE are both expressed within the BM microenvironment, being particularly evident in BM sinusoids and also small subsets of hematopoietic cells. Next, we took advantage of CD36 and ApoEKO models to study their hematological parameters and BM cellular contents. To do so, CD36/ApoEKO mice and their counterparts were euthanized and BM and peripheral blood cells were collected, stained for CD11b (myeloid cells), B220 (B lymphocytes), Sca1 (progenitor cells), Flk1 (endothelial cells) and analyzed by FACS. FACS analysis of BM cells revealed that KO and WT mice had similar progenitor cells and B lymphocytes percentage, but substantially less myeloid cells. Peripheral blood analysis revealed a substantial increase in circulating B lymphocytes, and a decrease in circulating progenitor cells and myeloid cells. Regarding circulating endothelial cells, no differences were detected between KO and WT mice. However, ApoEKO mice had increased levels of BM endothelial cells and progenitor cells. As B lymphocytes are increased in the periphery and diminished in the BM, CD36 deficiency (which results in diminished CH uptake) seems to promote B lymphocyte exit from the BM. An opposing effect seems to occur in the progenitor cell populations, since less percentage in the peripheral blood might imply a failure in their exit from the BM. Alternatively, altered CH levels may affect selectively progenitor cell (subsets) differentiation. In order to investigate the role of CH modulation in hematopoietic differentiation/commitment, progenitor cells (Lin-Sca+) from CD36 WT mice were cultured in a methylcellulose hematopoietic differentiation assay and also cultured in endothelial differentiation conditions in the presence/absence of a CH lowering agent (Pravastatin). At day 9 of differentiation, cells were collected and expression of Sca1, CD11b and Flk1 was analyzed by flow cytometry. Reduced CH availability, as a result of Pravastatin treatment, resulted in substantial lower levels of differentiated endothelial cells, suggesting a blockade in this differentiation process, and in a reduced number of progenitor cells, suggesting progenitor cell death. Notably, the percentage of myeloid cells was not affected by Pravastatin treatment. Taken together, we suggest that CH influences not only trafficking between BM and peripheral blood, influences endothelial cell differentiation, and might also influence BM recovery to injury by diminishing progenitor cell number available for subsequent hematopoiesis. Current studies aim at comparing the BM hematopoietic recovery of CD36, ApoEKO vs control in response to sublethal irradiation, and the contribution of the BM endothelial compartment in this process.

Repeated Hematopoietic Stem and Progenitor Cell Mobilization Without Depletion of the Bone Marrow Stem and Progenitor Cell Pool in Mice After Repeated Administration of Recombinant Murine G-CSF

2007 ◽  
Vol 68 (5) ◽  
pp. 368-374 ◽  
Author(s):  
Evert-Jan F.M. de Kruijf ◽  
Melissa van Pel ◽  
Henny Hagoort ◽  
Donnée Kruysdijk ◽  
Graham Molineux ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cell ◽  
Repeated Administration ◽  
Hematopoietic Stem ◽  
Cell Pool ◽  
Cell Mobilization ◽  
Progenitor Cell Pool

scholarly journals Dopamine regulates endothelial progenitor cell mobilization from mouse bone marrow in tumor vascularization

2008 ◽  
Vol 118 (4) ◽  
pp. 1380-1389 ◽  
Author(s):  
Debanjan Chakroborty ◽  
Uttio Roy Chowdhury ◽  
Chandrani Sarkar ◽  
Rathindranath Baral ◽  
Partha Sarathi Dasgupta ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Mouse Bone Marrow ◽  
Tumor Vascularization ◽  
Endothelial Progenitor ◽  
Cell Mobilization

scholarly journals Identification of Free Nitric Oxide Radicals in Rat Bone Marrow: Implications for Progenitor Cell Mobilization in Hypertension

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e57761 ◽  
Author(s):  
Marina A. Aleksinskaya ◽  
Ernst E. H. van Faassen ◽  
Jelly Nelissen ◽  
Ben J. A. Janssen ◽  
Jo G. R. De Mey ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bone Marrow ◽  
Progenitor Cell ◽  
Cell Mobilization ◽  
Rat Bone

Identification of Quantitative Trait Loci Regulating Steady State Hematopoiesis and Progenitor Mobilization in AKRB6F2 Mice.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4165-4165
Author(s):  
Ronald van Os ◽  
Albertina Ausema ◽  
Edo Vellenga ◽  
Gerald de Haan
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Progenitor Cell ◽  
Stem Cell Mobilization ◽  
Hematopoietic System ◽  
Cell Numbers ◽  
Trait Loci ◽  
Cell Mobilization

Abstract The hematopoietic system is a complex organized tissue with a hierarchical structure. Identification of organizational pathways within the hematopoietic system would be relevant for a better understanding of hematopoiesis in health and disease. We have analyzed numerous hematopoietic parameters in AKRB6F2 mice, a cross between AKR and C57Bl/6 mice that differ in various stem cell traits. Specifically, we have measured stem cell numbers, progenitor cell cycling, G-CSF induced stem cell mobilization, as well as neutrophil numbers in blood and bone marrow. We used these data to map quantitative trait loci for these parameters in order to assess whether distinct traits are associated with each other and by which genetic loci these parameters are regulated. When the different hematopoietic parameters were compared, surprisingly few significant correlations were found and only two quantitative trait loci (QTL) could be identified for all hematopoietic parameters. We confirm that a region on chromosome 11 is involved in progenitor cell cycling and we found an additional QTL for stem cell numbers, measured as CAFC day 35 per femur, on chromosome 2. A suggestive QTL was found for the number of progenitors in the bone marrow and the number of neutrophils in the blood. In the first of two series of offspring mice we found a strong association between stem cell mobilization and B6 alleles at the chromosome 3 locus D3Mit88 or AKR alleles on chromosome 15 (D15Mit241). However, this could not be confirmed in the second series. In addition, breeding of an F3 generation from the best mobilizers (6479 ± 1544 CFU-GM/ml blood vs. 3481 ± 3076 overall) of each series did not result in high mobilization capacity of the offspring (1333 ± 844 CFU-GM/ml). Taken together, our data illustrates that different hematopoietic parameters are independently regulated. This suggests that hematopoiesis is highly structured and regulation at all levels of stem cell development can lead to distinct mechanisms of stem cell maintenance resulting in normal levels of mature blood cells. Additionally, variation based on epigenetic determinants that do not transmit to the next generation may play an important role in the regulation of steady state hematopoiesis and stem cell mobilization.

scholarly journals Mobilization of CD34+ Progenitor Cells in Association with Decreased Proliferation in the Bone Marrow of Macaques after Administration of the Fms-Like Tyrosine Kinase 3 Ligand

2010 ◽  
Vol 17 (8) ◽  
pp. 1269-1273 ◽  
Author(s):  
R. Keith Reeves ◽  
Qing Wei ◽  
Patricia N. Fultz
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Tyrosine Kinase ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Flow Cytometric ◽  
Progenitor Cell Proliferation ◽  
Cell Mobilization ◽  
Negative Regulatory Mechanism

ABSTRACT Fms-like tyrosine kinase 3 ligand (FLT3-L) is critical for the differentiation and self-renewal of CD34+ progenitor cells in primates and has been used therapeutically to mobilize progenitor and dendritic cells in vivo. However, little is known regarding the expansion of progenitor cells outside of peripheral blood, particularly in bone marrow (BM), where progenitor cells primarily reside. Evaluation of FLT3-L-mediated cell mobilization during lentivirus infections, where the numbers of CD34+ progenitor cells are reduced, is limited. We enumerated frequencies and absolute numbers of CD34+ progenitor cells in blood and BM of naive and SIV- or SHIV-infected macaques during and after the administration of FLT3-L. Flow cytometric analyses revealed that, while CD34+ cells increased in the circulation, no expansion was observed in BM. Furthermore, in the BM intracellular Ki67, a marker of cell proliferation, was downregulated in CD34+ progenitor cells but was upregulated significantly in the bulk cell population. Although the exact mechanism(s) remains unclear, these data suggest that CD34+ cell mobilization in blood was the result of cellular emigration from BM and not the proliferation of CD34+ cells already in the periphery. It is possible that the decreased progenitor cell proliferation observed in BM is evidence of a negative regulatory mechanism preventing hyperproliferation and development of neoplastic cells.

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