scholarly journals G-CSF and/or M-CSF accelerate differentiation of bone marrow cells into endothelial progenitor cells in vitro

2006 ◽  
Author(s):  
Yuming Zhang ◽  
Yasushi Adachi ◽  
Masayoshi Iwasaki ◽  
Keizo Minamino ◽  
Yasuhiro Suzuki ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Bone Marrow Cells ◽  
Endothelial Progenitor ◽  
Marrow Cells

scholarly journals Reduced Ischemic Brain Injury by Partial Rejuvenation of Bone Marrow Cells in Aged Rats

2010 ◽  
Vol 31 (3) ◽  
pp. 855-867 ◽  
Author(s):  
Akihiko Taguchi ◽  
Pengxiang Zhu ◽  
Fang Cao ◽  
Akie Kikuchi-Taura ◽  
Yukiko Kasahara ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Bone Marrow Cells ◽  
Aged Rats ◽  
Endothelial Progenitor ◽  
Ischemic Brain ◽  
Marrow Cells

Circulating bone marrow-derived immature cells, including endothelial progenitor cells, have been implicated in homeostasis of the microvasculature. Decreased levels of circulating endothelial progenitor cells, associated with aging and/or cardiovascular risk factors, correlate with poor clinical outcomes in a range of cardiovascular diseases. Herein, we transplanted bone marrow cells from young stroke-prone spontaneously hypertensive rats (SHR-SP) into aged SHR-SP, the latter not exposed to radiation or chemotherapy. Analysis of recipient peripheral blood 28 days after transplantation revealed that 5% of circulating blood cells were of donor origin. Cerebral infarction was induced on day 30 posttransplantation. Animals transplanted with bone marrow from young SHR-SP displayed an increase in density of the microvasculature in the periinfarction zone, reduced ischemic brain damage and improved neurologic function. In vitro analysis revealed enhanced activation of endothelial nitric oxide synthase and reduced activation p38 microtubule-associated protein (MAP) kinase, the latter associated with endothelial apoptosis, in cultures exposed to bone marrow-derived mononuclear cells from young animals versus cells from aged counterparts. Our findings indicate that partial rejuvenation of bone marrow from aged rats with cells from young animals enhances the response to ischemic injury, potentially at the level of endothelial/vascular activation, providing insight into a novel approach ameliorate chronic vascular diseases.

scholarly journals Expansion of Endothelial Progenitor Cells in High Density Dot Culture of Rat Bone Marrow Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107127 ◽  
Author(s):  
Yang Lu ◽  
Yiyi Gong ◽  
Jie Lian ◽  
Ling Wang ◽  
James D. Kretlow ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Bone Marrow Cells ◽  
High Density ◽  
Endothelial Progenitor ◽  
Rat Bone ◽  
Marrow Cells

Determine exogenous humanDDAH2gene function in rabbit bone marrow-derived endothelial progenitor cells in vitro

2017 ◽  
Vol 35 (2) ◽  
pp. 69-76
Author(s):  
Sara Shoeibi ◽  
Shabnam Mohammadi ◽  
Hamid Reza Sadeghnia ◽  
Elahe Mahdipour ◽  
Majid Ghayour-Mobarhan
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Rabbit Bone

Enhanced endothelialization and microvessel formation in polyester grafts seeded with CD34+ bone marrow cells

Blood ◽  
2000 ◽  
Vol 95 (2) ◽  
pp. 581-585 ◽  
Author(s):  
Vishwanath Bhattacharya ◽  
Peter A. McSweeney ◽  
Qun Shi ◽  
Benedetto Bruno ◽  
Atsushi Ishida ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Vascular Graft ◽  
Bone Marrow Cells ◽  
Venous Blood ◽  
Immunomagnetic Bead ◽  
Composite Grafts ◽  
Cd34 Cells ◽  
Marrow Cells

The authors have shown accelerated endothelialization on polyethylene terephthalate (PET) grafts preclotted with autologous bone marrow. Bone marrow cells have a subset of early progenitor cells that express the CD34 antigen on their surfaces. A recent in vitro study has shown that CD34+ cells can differentiate into endothelial cells. The current study was designed to determine whether CD34+ progenitor cells would enhance vascular graft healing in a canine model. The authors used composite grafts implanted in the dog's descending thoracic aorta (DTA) for 4 weeks. The 8-mm × 12-cm composite grafts had a 4-cm PET graft in the center and 4-cm standard ePTFE grafts at each end. The entire composite was coated with silicone rubber to make it impervious; thus, the PET segment was shielded from perigraft and pannus ingrowth. There were 5 study grafts and 5 control grafts. On the day before surgery, 120 mL bone marrow was aspirated, and CD34+ cells were enriched using an immunomagnetic bead technique, yielding an average of 11.4 ± 5.3 × 106. During surgery, these cells were mixed with venous blood and seeded onto the PET segment of composite study grafts; the control grafts were treated with venous blood only. Hematoxylin and eosin, immunocytochemical, and AgNO3staining demonstrated significant increases of surface endothelialization on the seeded grafts (92% ± 3.4% vs 26.6% ± 7.6%; P = .0001) with markedly increased microvessels in the neointima, graft wall, and external area compared with controls. In dogs, CD34+ cell seeding enhances vascular graft endothelialization; this suggests practical therapeutic applications.

Requirement for p85α Regulatory Subunit of Class IA PI3Kinase and Rac2 GTPase in Myeloproliferative Disease Driven by Activation Loop Mutant of KIT.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 89-89
Author(s):  
Veerendra Munugalavadla ◽  
Emily C. Sims ◽  
Stephen D. Lenz ◽  
Reuben Kapur
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Progenitor Cells ◽  
Bone Marrow Cells ◽  
Regulatory Subunit ◽  
Activation Loop ◽  
Myeloproliferative Disease ◽  
Hematopoietic Stem ◽  
Marrow Cells

Abstract Oncogenic activation-loop mutants of KIT, the receptor for stem cell factor (SCF), are commonly observed in acute myeloid leukemia (AML) and systemic mastocytosis (SM); however, unlike the KIT juxtamembrane mutants (found in patients with gastrointestinal stromal tumors [GISTs]), the activation-loop mutants are commonly insensitive to inhibition by tyrosine kinase inhibitors. Furthermore, little is known about the signaling pathways that contribute to oncogenic KIT-induced transformation in SM or AML. We demonstrate that expression of KITD814V (KIT activation-loop mutant) in primary hematopoietic stem and progenitor cells induces constitutive KIT autophosphorylation, promotes ligand-independent hyperproliferation, skews myeloid differentiation towards the granulocytic lineage, and promotes promiscuous cooperation with multiple cytokines, including G-CSF, M-CSF and IL-3. KITD814V expressing primary mast cells also demonstrated hyperproliferation in response to SCF, IL-3, IL-4 and IL-10. Biochemical analyses of KITD814V expressing cells revealed constitutively elevated levels of phosphatidylinositol-3-kinase (PI3K) and its downstream substrate, the Rho family GTPase Rac. Genetic disruption of p85a, the regulatory subunit of class IA PI-3Kinase, but not of p85β, or genetic disruption of the hematopoietic cell-specific Rho GTPase, Rac2, normalized KITD814V-induced ligand independent hyperproliferation in vitro. Additionally, deficiency of p85α or Rac2 corrected the promiscuous hyperproliferation observed in response to multiple cytokines in both KITD814V expressing stem/progenitor cells as well as mast cells in vitro. Although p85α is hyperphosphorylated and constitutively bound to KITD814V in bone marrow cells in vitro; its physiologic role in transformation in vivo is not known. To address this, we generated a new mouse model to study KITD814V induced transformation in myeloid cells as opposed to previously described models that primarily result in the generation of phenotypes resembling acute lymphocytic leukemia via this mutation. Our results show that transplantation of KITD814V expressing bone marrow cells from C57/BL6 strain of mice into syngeneic recipients results in a fatal myeloproliferative disease (MPD) characterized by leukocytosis, splenomegaly, disruption of the splenic architecture as well as myeloid cell infiltration in the lung and liver. Importantly, in this model, transplantation of KITD814V expressing p85α deficient bone marrow cells rescued the MPD phenotype, including splenomegaly, peripheral blood leukocytosis and the reduced life span associated with the transplantation of KITD814V expressing wildtype bone marrow cells. Treatment of KITD814V-expressing hematopoietic progenitors with either a Rac inhibitor (NC23766) or rapamycin showed a dose-dependent suppression in KITD814V induced growth. Taken together, our results describe the generation of a new murine transplant model to study KITD814V induced transformation and identify p85a and Rac2 as potential novel therapeutic target for the treatment of KITD814V-bearing diseases including SM and AML.

scholarly journals A new method of culturing rat bone marrow endothelial progenitor cells in vitro

2020 ◽  
Vol 10 (5) ◽  
pp. 1270-1279
Author(s):  
Zhaohong Kong ◽  
Meixin Chen ◽  
Jian Jiang ◽  
Jiang Zhu ◽  
Yumin Liu
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
New Method ◽  
Endothelial Progenitor ◽  
Rat Bone

Diabetes alters subsets of endothelial progenitor cells that reside in blood, bone marrow, and spleen

2012 ◽  
Vol 302 (6) ◽  
pp. C892-C901 ◽  
Author(s):  
Hidehito Saito ◽  
Yasuhiko Yamamoto ◽  
Hiroshi Yamamoto
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Insulin Treatment ◽  
Vascular Complications ◽  
Cell Number ◽  
Surface Marker ◽  
Endothelial Progenitor ◽  
Marker Combination

Circulating endothelial progenitor cells (EPCs) derived from the bone marrow (BM) participate in maintaining endothelial integrity and vascular homeostasis. Reduced EPC number and function result in vascular complications in diabetes. EPCs are a population of cells existing in various differentiation stages, and their cell surface marker profiles change during the process of mobilization and maturation. Hence, a generally accepted marker combination and a standardized protocol for the quantification of EPCs remain to be established. To determine the EPC subsets that are affected by diabetes, we comprehensively analyzed 32 surface marker combinations of mouse peripheral blood (PB), BM, and spleen cells by multicolor flow cytometry. Ten subsets equivalent to previously reported mouse EPCs significantly declined in number in the PB of streptozotocin-induced diabetic mice, and this reduction was reversed by insulin treatment. The PI−Lin−c-Kit−Sca-1+Flk-1−CD34−CD31+ EPC cluster, which can differentiate into mature endothelial cells in vitro, was the highest population in the PB, BM, and spleen and occurred 61 times more in the spleen than in the PB. The cell number significantly decreased in the BM as well as in the PB but paradoxically increased in the spleen under diabetic conditions. Insulin treatment reversed the decrease of EPC subsets in the BM and PB and reversed their increase in spleen. A similar tendency was observed in some of the major cell populations in db/db mice. To the best of our knowledge, we are the first to report spatial population changes in mouse EPCs by diabetes in the blood and in the BM across the spleen. Diminished circulating EPC supply by diabetes may be ascribed to impaired EPC production in the BM and to decreased EPC mobilization from the spleen, which may contribute to vascular dysfunction in diabetic conditions.

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