scholarly journals Efficient nano iron particle-labeling and noninvasive MR imaging of mouse bone marrow-derived endothelial progenitor cells

2011 ◽  
pp. 511 ◽  
Author(s):  
Chen ◽  
Jia
Keyword(s):  
Bone Marrow ◽  
Mr Imaging ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Iron Particle ◽  
Mouse Bone Marrow ◽  
Endothelial Progenitor

Gleevec and Rapamycin Synergistically Reduce Cell Viability and Inhibit Proliferation and Angiogenic Function of Mouse Bone Marrow-Derived Endothelial Progenitor Cells

2021 ◽  
pp. 1-12
Author(s):  
Ling Chen ◽  
Luping Dai ◽  
Dewen Yan ◽  
Boya Zhou ◽  
Wei Zheng ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Cell Apoptosis ◽  
Tube Formation ◽  
Endothelial Differentiation ◽  
Mouse Bone Marrow ◽  
Endothelial Progenitor

<b><i>Objective:</i></b> This study investigates the synergistic effects of Gleevec (imatinib) and rapamycin on the proliferative and angiogenic properties of mouse bone marrow-derived endothelial progenitor cells (EPCs). <b><i>Materials and Methods:</i></b> EPCs were isolated from mouse bone marrow and treated with different concentrations of Gleevec or rapamycin individually or in combination. The cell viability and proliferation were examined using the MTT assay. An analysis of cell cycle and apoptosis was performed using flow cytometry. Formation of capillary-like tubes was examined in vitro, and the protein expression of cell differentiation markers was determined using Western blot analysis. <b><i>Results:</i></b> Gleevec significantly reduced cell viability, cell proliferation, and induced cell apoptosis in EPCs. Rapamycin had similar effects on EPCs, but it did not induce cell apoptosis. The combination of Gleevec and rapamycin reduced the cell proliferation but increased cell apoptosis. Although rapamycin had no demonstratable effect on tube formation, the combined therapy of Gleevec and rapamycin significantly reduced tube formation when compared with Gleevec alone. Mechanistically, Gleevec, but not rapamycin, induced a significant elevation in caspase-3 activity in EPCs, and it attenuated the expression of the endothelial protein marker platelet-derived growth factor receptor α. Functionally, rapamycin, but not Gleevec, significantly enhanced the expression of endothelial differentiation marker proteins, while attenuating the expression of mammalian target of rapamycin signaling-related proteins. <b><i>Conclusions:</i></b> Gleevec and rapamycin synergistically suppress cell proliferation and tube formation of EPCs by inducing cell apoptosis and endothelial differentiation. Mechanistically, it is likely that rapamycin enhances the proapoptotic and antiangiogenic effects of Gleevec by promoting the endothelial differentiation of EPCs. Given that EPCs are involved in the pathogenesis of some cardiovascular diseases and critical to angiogenesis, pharmacological inhibition of EPC proliferation by combined Gleevec and rapamycin therapy may be a promising approach for suppressing cardiovascular disease pathologies associated with angiogenesis.

scholarly journals Mouse Bone Marrow-Derived Endothelial Progenitor Cells Do Not Restore Radiation-Induced Microvascular Damage

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Ingar Seemann ◽  
Johannes A. M. te Poele ◽  
Saske Hoving ◽  
Fiona A. Stewart
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Damage ◽  
Endothelial Cell Proliferation ◽  
Mouse Bone Marrow ◽  
Endothelial Progenitor ◽  
Microvascular Damage ◽  
Radiation Induced ◽  
Microvasculature Damage

Background. Radiotherapy is commonly used to treat breast and thoracic cancers but it also causes delayed microvascular damage and increases the risk of cardiac mortality. Endothelial cell proliferation and revascularization are crucial to restore microvasculature damage and maintain function of the irradiated heart. We have therefore examined the potential of bone marrow-derived endothelial progenitor cells (BM-derived EPCs) for restoration of radiation-induced microvascular damage. Material & Methods. 16 Gy was delivered to the heart of adult C57BL/6 mice. Mice were injected with BM-derived EPCs, obtained from Eng+/+ or Eng+/− mice, 16 weeks and 28 weeks after irradiation. Morphological damage was evaluated at 40 weeks in transplanted mice, relative to radiation only and age-matched controls. Results. Cardiac irradiation decreased microvascular density and increased endothelial damage in surviving capillaries (decrease alkaline phosphatase expression and increased von Willebrand factor). Microvascular damage was not diminished by treatment with BM-derived EPCs. However, BM-derived EPCs from both Eng+/+ and Eng+/− mice diminished radiation-induced collagen deposition. Conclusion. Treatment with BM-derived EPCs did not restore radiation-induced microvascular damage but it did inhibit fibrosis. Endoglin deficiency did not impair this process.

scholarly journals Improved Culture-Based Isolation of Differentiating Endothelial Progenitor Cells from Mouse Bone Marrow Mononuclear Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28639 ◽  
Author(s):  
Haruki Sekiguchi ◽  
Masaaki Ii ◽  
Kentaro Jujo ◽  
Ayumi Yokoyama ◽  
Nobuhisa Hagiwara ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Mouse Bone Marrow ◽  
Bone Marrow Mononuclear Cells ◽  
Endothelial Progenitor

Defined Populations of Bone Marrow Derived Mesenchymal Stem and Endothelial Progenitor Cells for Bladder Regeneration

2009 ◽  
Vol 182 (4S) ◽  
pp. 1898-1905 ◽  
Author(s):  
Arun K. Sharma ◽  
Natalie J. Fuller ◽  
Ryan R. Sullivan ◽  
Noreen Fulton ◽  
Partha V. Hota ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Bladder Regeneration

scholarly journals A PEDF-Derived Peptide Inhibits Retinal Neovascularization and Blocks Mobilization of Bone Marrow-Derived Endothelial Progenitor Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Richard Longeras ◽  
Krysten Farjo ◽  
Michael Ihnat ◽  
Jian-Xing Ma
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Pigment Epithelium ◽  
Retinal Neovascularization ◽  
Endothelial Progenitor ◽  
Amino Acid Peptide ◽  
Oxygen Induced Retinopathy ◽  
Pigment Epithelium Derived Factor ◽  
Circulating Endothelial Progenitor Cells

Proliferative diabetic retinopathy is characterized by pathological retinal neovascularization, mediated by both angiogenesis (involving mature endothelial cells) and vasculogenesis (involving bone marrow-derived circulating endothelial progenitor cells (EPCs)). Pigment epithelium-derived factor (PEDF) contains an N-terminal 34-amino acid peptide (PEDF-34) that has antiangiogenic properties. Herein, we present a novel finding that PEDF-34 also possesses antivasculogenic activity. In the oxygen-induced retinopathy (OIR) model using transgenic mice that have Tie2 promoter-driven GFP expression, we quantified Tie2GFP+cells in bone marrow and peripheral blood by fluorescence-activated cell sorting (FACS). OIR significantly increased the number of circulating Tie2-GFP+at P16, correlating with the peak progression of neovascularization. Daily intraperitoneal injections of PEDF-34 into OIR mice decreased the number of Tie2-GFP+cells in the circulation at P16 by 65% but did not affect the number of Tie2-GFP+cells in the bone marrow. These studies suggest that PEDF-34 attenuates EPC mobilization from the bone marrow into the blood circulation during retinal neovascularization.

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