The influence of a solid tumor of the mouse on the proliferation kinetics of haemopoietic bone marrow cells

1984 ◽  
Vol 107 (3) ◽  
pp. 164-168
Author(s):  
W. F�aux de Lacroix ◽  
B. Buran-Kilian
Keyword(s):  
Bone Marrow ◽  
Solid Tumor ◽  
Bone Marrow Cells ◽  
Proliferation Kinetics ◽  
Kinetics Of ◽  
Marrow Cells

The kinetics of in vivo sister chromatid exchange induction in mouse bone marrow cells by ethylnitrosourea and methylnitrosourea

1986 ◽  
Vol 84 (1) ◽  
pp. 56-65 ◽  
Author(s):  
James L. Charles ◽  
David Jacobson-Kram ◽  
Lyman W. Condie ◽  
Joseph F. Borzelleca ◽  
Richard A. Carchman
Keyword(s):  
Bone Marrow ◽  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Bone Marrow Cells ◽  
Mouse Bone Marrow ◽  
Kinetics Of ◽  
Mouse Bone Marrow Cells ◽  
Marrow Cells

scholarly journals Monocyte-derived recruiting activity: kinetics of production and effects of endotoxin

Blood ◽  
1985 ◽  
Vol 65 (3) ◽  
pp. 689-695 ◽  
Author(s):  
E McCall ◽  
GC Jr Bagby
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Bone Marrow Cells ◽  
Umbilical Vein ◽  
Calf Serum ◽  
Fold Increase ◽  
Umbilical Vein Endothelial Cells ◽  
Kinetics Of ◽  
Marrow Cells

Abstract Cultured monocytes release a factor, monocyte-derived recruiting activity (MRA), which stimulates fibroblasts, endothelial cells, and T lymphocytes to produce colony-stimulating activity (CSA). We studied the kinetics of MRA production using a technique in which MRA levels were measured in a two stage bioassay. We used umbilical vein endothelial cells as the MRA-responsive (CSA-producing) cells, and normal colony-forming unit granulocyte-macrophage (CFU-GM)-enriched bone marrow cells (T lymphocyte- and monocyte-depleted, low density bone marrow cells) as the CSA-responsive cells. MRA stimulated a 30- fold increase in CSA production by endothelial cells. MRA production was detected in supernatants from as few as 10(3) monocytes per milliliter, required the presence of fetal calf serum, and was inhibited by cycloheximide (10 to 100 micrograms/mL) and puromycin (10 to 50 micrograms/mL). Production was detectable after 24 hours of monocyte incubation, was maintained for three days, and fell to undetectable levels by seven days. With the addition of bacterial endotoxin (lipopolysaccharide [LPS]) (50 micrograms per 10(6) cells), MRA was detectable after only three hours of incubation, and levels peaked at 24 hours. Further, maximum MRA levels in the supernatants of LPS-stimulated monocytes were up to ten times greater than peak levels in the supernatants of unstimulated monocytes. Endotoxin augmented monocyte production of MRA to a greater extent than it did CSA production, indicating that the stimulation of CSA production by endotoxin may be at least partly indirect. The responsiveness of MRA production to endotoxin in vitro is consistent with the notion that MRA may be a biologically relevant regulator of CSA production by cells of the hematopoietic microenvironment.

scholarly journals In vivo investigations of clastogenic effect of levamisole hydrochloride on bone marrow cells of BALB/c mice

2005 ◽  
Vol 59 (5-6) ◽  
pp. 549-556
Author(s):  
Milan Kulic ◽  
Zoran Stanimirovic ◽  
Sinisa Ristic ◽  
Biljana Markovic
Keyword(s):  
Bone Marrow ◽  
Mitotic Activity ◽  
Opposite Effect ◽  
Bone Marrow Cells ◽  
The Other ◽  
Control Group ◽  
Clastogenic Effect ◽  
Kinetics Of ◽  
Marrow Cells

Cytotoxic and genotoxic examinations were performed of the effect of levamisole hydrochloride (2.2 mg/kg bm, 4.4 mg/kg bm, LD50-25% mg/kg bm and LD50-75% mg/kg bm) on bone marrow cells of mice of the BALB/c strain. The effect of levamisole hydrochloride on kinetics of the cellular cycle and the appearance of structural and numerical changes in chromosomes of bone marrow cells were followed. The therapeutic dose of levamisole of 2.2 mg/kg bm showed the ability to increase the mitotic activity of the observed cells, thus confirming knowledge of the immunostimulative effect of this dose of the medicine under in vivo conditions. The other tested doses of levamisole in this experiment, observed in comparison with the control group, had an opposite effect, i.e. they caused a reduction in the mitotic activity of bone marrow cells. All the examined doses in vivo showed the ability of inducing numeric (aneuloid and polyploid) and structural (lesions, breaks and insertions) chromosomal aberrations. On this basis, it can be concluded that the examined doses have a genotoxic effect.

Mad2 (Mitotic Arrest Deficiency 2) Is Essential for the Synergistic Proliferation Induced by Stem Cell Factor Combined with GM-CSF in Hematopoietic Progenitor Cells, Effects Reflecting the Association of c-kit with Mad2.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 71-71
Author(s):  
Shigeki Ito ◽  
Charlie Mantel ◽  
Myung-Kwan Han ◽  
Seiji Fukuda ◽  
Yoji Ishida ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Bone Marrow Cells ◽  
Cytokine Signaling ◽  
Mouse Bone Marrow ◽  
Wild Type ◽  
Gm Csf ◽  
Kinetics Of ◽  
Marrow Cells

Abstract Mitotic spindle checkpoint protein, Mad2, is required for proper functioning of the mitotic checkpoint which ensures correct chromosome segregation during cell division. Homozygous Mad2 gene deletion is embryonic-lethal. Mad2 interacts with mitosis-associated molecules such as Mad1 and anaphase promoting complex/cyclosome to ensure proper cell cycle progression. Recently, Mad2 was shown to physically associate with the common beta chain of the GM-CSF receptor which raises the possibility that Mad2 may also be involved in cytokine signaling and regulation of mitosis in hematopoietic progenitor cells. To investigate this, we studied hematopoiesis and cytokine signaling in Mad2-haploinsufficient (+/−) mutant mice (M2MT). Colony formation by granulocyte macrophage progenitor cells (CFU-GM) from bone marrow of wild type (WT) mice is synergistically stimulated in vitro by the combination of stem cell factor (SCF) and GM-CSF. We found that bone marrow CFU-GM from M2MT mice are deficient in the synergistic proliferative/colony formation response in vitro to stimulation with the combination of GM-CSF plus SCF. In contrast, there was no difference in stimulation of CFU-GM formation in response to the individual cytokines, GM-CSF or SCF alone, nor a difference in response to pokeweed mitogen mouse spleen cell conditioned medium between M2MT and WT mice. Because there was no difference in the frequency of c-kit+Sca-1+Lin- (KSL) cells nor a difference in the intensity of c-kit surface expression on KSL cells from wild type and M2MT mice, we considered whether the suppression of the SCF/GM-CSF synergy response was due to a difference in intracellular growth-factor receptor signaling pathways. We found that the kinetics of Erk1/2 phosphorylation signaling differ in M2MT Lin- cells compared to WT Lin- cells and that the duration of Erk1/2 phosphorylation in M2MT cells was at least one half of that in WT Lin- cells. On the other hand, we found no difference in the kinetics of Akt phosphorylation between WT and M2MT Lin- cells suggesting a specificity of involvement of the MAP-kinase pathways. To understand how Mad2 plays a role in SCF/GM-CSF synergy, we tested the physical interaction between Mad2 and c-kit in primary Lin- mouse bone marrow cells. Primary Lin- bone marrow cells from WT mice were expanded in liquid culture with SCF and thrombopoietin for 5 days. We found that Mad2 physically associated with c-kit as indicated by co-immunoprecipitation. These results suggest that Mad2 is required for the SCF/GM-CSF proliferative-synergy response in primary Lin- mouse bone marrow cells and that Mad2 is involved in growth-factor signaling pathways, such as the MAP-kinase cascade, in addition to spindle checkpoint function in primary hematopoietic cells. These effects are likely mediated through Mad2 interaction with c-kit and the beta chain of the GM-CSF receptor.

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