QUANTITATIVE STUDIES ON THE STIMULATION OF MOUSE BONE MARROW COLONY GROWTH IN VITRO BY NORMAL HUMAN URINE

1969 ◽  
Vol 47 (4) ◽  
pp. 453-466 ◽  
Author(s):  
D Metcalf ◽  
ER Stanley
Blood ◽  
1969 ◽  
Vol 33 (3) ◽  
pp. 396-399 ◽  
Author(s):  
W. A. ROBINSON ◽  
E. R. STANLEY ◽  
D. METCALF

Abstract Using a new technic of bone marrow culture in agar, urine samples from 50 humans have been tested for their ability to stimulate the formation of granulocyte—mononuclear cell growth in vitro. Significant colony stimulating activity has been found with 25 out of 50 unconcentrated urine samples from both normal humans and patients with a variety of disease states.


Blood ◽  
1976 ◽  
Vol 48 (4) ◽  
pp. 601-608 ◽  
Author(s):  
FD Wilson ◽  
L O'Grady

Abstract Studies on the mechanism of anemia in mice of genotype S1/S1d have implicated the hematopoietic stroma (the hematopoietic inductive microenvironment, HIM) rather than hematopoietic stem cells as the site of the defect. Using methylcellulose-supported bone marrow culture systems, we have observed, in addition to classical hematopoietic colonies, the formation of surface associated fibroblastic plaques that could stimulate hematopoietic colony growth. These plaques were hypothesized to be derived from bone marrow stroma precursors. In view of the reported stromal-based defect in S1/S1d mice, studies were initiated, using our culture system, to determine if abnormalities exist in the plaque-forming potentials of these mice. Relative to controls, bone marrow derived from S1/S1d mice exhibited a significant decrease in hematopoietic colonly-forming units in culture, but no differences were apparent in the absolute numbers of fibroblastic plaque-forming units or in the ability of such plaques once derived to stimulate hematopoietic colony growth when overlain with fresh normal bone marrow preparations. Quantitative studies on the bone marrow of the S1/S1d mice revealed a marked reduction in total nucleated cells per femur. The importance of evaluating the results of bone marrow cultures in an absolute (i.e., number of units per femur) rather than a relative (i.e., number of units forming in a constant cell inoculum) term was underlined by these studies.


Blood ◽  
1980 ◽  
Vol 56 (4) ◽  
pp. 706-711 ◽  
Author(s):  
SH Bartelmez ◽  
WH Dodge ◽  
AA Mahmoud ◽  
DA Bass

Abstract Eosinophilopoietin (EPP) was previously characterized by the ability to stimulate eosinophil production in vivo, but these studies could not ascertain whether EPP had a direct effect on the bone marrow or acted indirectly by causing release of eosinophilopoietic activity by other tissues. The present studies demonstrate that EPP stimulates eosinophil growth in liquid culture of mouse bone marrow in vitro. The timing of stimulation by EPP in vivo and in vitro were parallel, with maximal eosinophil growth after 48 hr. Moreover, EPP appears similar to, and possible identical with, the eosinophil growth-stimulating substance (EO-GSF) released by antigenic stimulation of immune nonadherent spleen cells. Both EPP and EO-GSF are of low molecular weight, both produce stimulation of eosinophil growth with identical kinetics, and both produced similar dose-response curves in the liquid culture system.


Blood ◽  
1976 ◽  
Vol 48 (4) ◽  
pp. 601-608
Author(s):  
FD Wilson ◽  
L O'Grady

Studies on the mechanism of anemia in mice of genotype S1/S1d have implicated the hematopoietic stroma (the hematopoietic inductive microenvironment, HIM) rather than hematopoietic stem cells as the site of the defect. Using methylcellulose-supported bone marrow culture systems, we have observed, in addition to classical hematopoietic colonies, the formation of surface associated fibroblastic plaques that could stimulate hematopoietic colony growth. These plaques were hypothesized to be derived from bone marrow stroma precursors. In view of the reported stromal-based defect in S1/S1d mice, studies were initiated, using our culture system, to determine if abnormalities exist in the plaque-forming potentials of these mice. Relative to controls, bone marrow derived from S1/S1d mice exhibited a significant decrease in hematopoietic colonly-forming units in culture, but no differences were apparent in the absolute numbers of fibroblastic plaque-forming units or in the ability of such plaques once derived to stimulate hematopoietic colony growth when overlain with fresh normal bone marrow preparations. Quantitative studies on the bone marrow of the S1/S1d mice revealed a marked reduction in total nucleated cells per femur. The importance of evaluating the results of bone marrow cultures in an absolute (i.e., number of units per femur) rather than a relative (i.e., number of units forming in a constant cell inoculum) term was underlined by these studies.


Blood ◽  
1971 ◽  
Vol 37 (2) ◽  
pp. 231-239 ◽  
Author(s):  
AHUVA KNYSZYNSKI ◽  
M. BURGER

Abstract Some characteristics of a bone marrow factor were ascertained, on the basis of its ability to increase 3H-thymidine incorporation into thymic cells in vitro. It was found that the factor was not detectable in kidney or spleen preparations derived from the same mice from which active bone marrow preparations were obtained. The activity of the factor was reduced shortly after total-body irradiation of the mice, and increased again during the regeneration of the bone marrow. It is further shown here that the bone marrow factor has no effect on 3H-thymidine incorporation into mouse bone marrow cells. Leukemic mouse thymic cells show a significantly reduced response towards the bone marrow factor in comparison to normal thymic cells. The bone marrow factor has less effect on protein synthesis than on DNA synthesis in thymic cells, and its stimulatory effect on DNA synthesis is not dependent on protein synthesis. The isolated bone marrow factor is resistant towards heating at 100°C, even at a very low or very high pH. However, it is more labile to heat when in an impure state. Its activity is not affected by RNase, DNase, pronase and carboxypeptidase. It is insoluble in ether, but soluble in absolute ethanol.


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