Macrophage-Inflammatory Protein Protects Multipotent Hematopoietic Cells From the Cytotoxic Effects of Hydroxyurea In Vivo

Macrophage-Inflammatory Protein Protects Multipotent Hematopoietic Cells From the Cytotoxic Effects of Hydroxyurea In Vivo

Macrophage inflammatory protein-1 α (MIP-1α) has been assessed for its potential in vivo to protect hematopoietic progenitor cells from the cytotoxic effects of a cycle-specific drug—in this case hydroxyurea (HU). Two doses of HU, 7 hours apart, were administered to mice to induce spleen colony-form...

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Bibliographic Details
Published in:Blood Vol. 79; no. 10; pp. 2605 - 2609
Main Authors: Lord, B.l., Dexter, T.M., Clements, J.M., Hunter, M.A., Gearing, A.J.H.
Format: Journal Article
Language:English
Published: Washington, DC Elsevier Inc 15-05-1992
The Americain Society of Hematology
Subjects:
Animals
Biological and medical sciences
Bone Marrow - pathology
Cell differentiation, maturation, development, hematopoiesis
Cell physiology
Cells, Cultured
Chemokine CCL4
Colony-Forming Units Assay
Cytokines - pharmacology
Female
Fundamental and applied biological sciences. Psychology
Hematopoietic Stem Cells - drug effects
Hematopoietic Stem Cells - pathology
Hydroxyurea - toxicity
Kinetics
Macrophage Inflammatory Proteins
Mice
Mice, Inbred Strains
Molecular and cellular biology
Monokines - pharmacology
Recombinant Proteins - pharmacology
Time Factors
Stem cell
Rodentia
Hematopoietic cell
Cytotoxicity
CFU-S-Cell
In vivo
Vertebrata
Chemotherapy
Mammalia
Mouse
Hematopoiesis
Animal
Macrophage
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Summary:Macrophage inflammatory protein-1 α (MIP-1α) has been assessed for its potential in vivo to protect hematopoietic progenitor cells from the cytotoxic effects of a cycle-specific drug—in this case hydroxyurea (HU). Two doses of HU, 7 hours apart, were administered to mice to induce spleen colony-forming unit (CFU-S) cycling and then to kill them during DNA-synthesis. MIP-1α, in a variety of dose and time combinations, was injected before the second dose of HU in an attempt to prevent recruitment or maintain CFU-S quies- cence, and thus protect them from the second dose of HU. Without MIP-lα, recovery of the CFU-S population was complete in 7 days. In a dose-dependent manner, MIP-1α either reduced the initial kill and accelerated recovery, or completely protected the CFU-S population. We conclude that MIP-1αdoes protect multipotent progenitor cells in vivo and that these observations provide a base from which to build practical clinical applications. © 1992 by The American Society of Hematology.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V79.10.2605.2605