|
|
Previous Article | Table of Contents | Next Article 
Synergistic effect of granulocyte colony-stimulating factor and drugs
elevating extracellular adenosine on neutrophil production in mice
M Pospisil, M Hofer, V Znojil, J Vacha, J Netikova and J Hola
Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno,
Czech Republic.
Experimental evidence suggests that the activation of purinoceptors by
extracellular adenosine can modulate proliferation and/or differentiation
of hematopoietic cells. The present study was undertaken to investigate the
potential interactions of this system of intercellular signaling with the
effects of granulocyte colony- stimulating factor (G-CSF) on granulopoiesis
in vivo. Elevation of extracellular adenosine in normal mice was induced by
the joined administration of dipyridamole, a drug inhibiting the cellular
uptake of adenosine, and adenosine monophosphate (AMP), an adenosine
prodrug. The effects of dipyridamole, AMP, and G-CSF, administered either
alone or in combinations, were evaluated. The agents were injected to mice
in a 4-day regimen, and the hematologic endpoints were determined 24 hours
after the completion of the treatment. It was shown that the effects of
G-CSF, ie, increases in peripheral blood neutrophils, granulocyte-
macrophage progenitor cells (GM-CFC), and morphologically determined
granulocytic cells in femoral marrow and a decrease in the marrow erythroid
cells, can be enhanced by the combination of dipyridamole plus AMP
administered 30 minutes before G-CSF. Furthermore, it was ascertained that
the stimulatory action of dipyridamole plus AMP was expressed particularly
at lower doses of G-CSF (1.5, 3, and 4.5 micrograms/d). At higher doses of
G-CSF (6 and 9 micrograms/d), the interactions were no more evident. When
combining dipyridamole, AMP, and 3 micrograms of G-CSF, peripheral
neutrophils increased approximately 3.9- to 4.5-fold compared with an
approximate 2.2-fold increase induced by G-CSF alone. The results indicate
the possible therapeutic potential of combination therapy with G-CSF and
drugs increasing extracellular adenosine.
Volume 86,
Issue 10,
pp. 3692-3697,
11/15/1995
Copyright © 1995 by The American Society of Hematology

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
M. Hofer, M. Pospisil, V. Znojil, J. Hola, D. Streitova, and A. Vacek
Homeostatic Action of Adenosine A3 and A1 Receptor Agonists on Proliferation of Hematopoietic Precursor Cells
Experimental Biology and Medicine,
July 1, 2008;
233(7):
897 - 900.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. S. Chang, R. Santhanam, R. Trotta, P. Neviani, A. M. Eiring, E. Briercheck, M. Ronchetti, D. C. Roy, B. Calabretta, M. A. Caligiuri, et al.
High levels of the BCR/ABL oncoprotein are required for the MAPK-hnRNP-E2 dependent suppression of C/EBP{alpha}-driven myeloid differentiation
Blood,
August 1, 2007;
110(3):
994 - 1003.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|
|