Macrophage inflammatory protein-1α receptors are present on cells enriched for CD34 expression from patients with chronic myeloid leukemia

Richard C. Chasty, Guy S. Lucas, P. Jane Owen-Lynch, Andrew Pierce, Anthony D. Whetton

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The response of normal and chronic myeloid leukemia (CML), CD34+cells to human macrophage inflammatory protein-1α (MIP-1α or LD78) was assessed. In tritiated thymidine incorporation assays, stem cell factor plus granulocyte- macrophage colony-stimulating factor stimulated thymidine incorporation in normal CD34+cells was reduced to 72% of control values in the presence of MIP-1α, whereas incorporation by CML CD34+cells exposed to the same factors was not altered. In clonogenic assays, the presence of MIP-1α gave a level of colony formation that was 71% of control values for normal progenitor cells, whereas for CML CD34+cells colony formation was enhanced by 25%. These results suggest that, in vitro, CML progenitor cells are relatively refractory to the growth inhibitory effects of MIP-1α. Using flow cytometry, the specific binding of a biotinylated human MIP-1α/avidin fluorescein (FITC) conjugate to normal and CML mononuclear and CD34+cell populations was quantified. The data indicate that (for both normal and CML CD34+cells) there was a single population of cells that express cell surface receptors for MIP-1α and this receptor expression was independent of cell cycle status. CML progenitor cells may be refractory to the effects of MIP-1α as a result of events downstream from receptor expression.
LanguageEnglish
Pages4270-4277
Number of pages8
JournalBlood
Volume86
Issue number11
Publication statusPublished - 1 Dec 1995
Externally publishedYes

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Chemokine CCL3
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Myeloid Progenitor Cells
Cells
Refractory materials
Thymidine
Assays
Macrophage Inflammatory Proteins
Stem Cell Factor
Flow cytometry
Fluorescein-5-isothiocyanate
Cell Surface Receptors
Granulocyte-Macrophage Colony-Stimulating Factor
macrophage inflammatory protein 1alpha receptor
Population
Cell Cycle
Flow Cytometry
Reference Values
Stem Cells
Growth

Cite this

Chasty, Richard C. ; Lucas, Guy S. ; Owen-Lynch, P. Jane ; Pierce, Andrew ; Whetton, Anthony D. / Macrophage inflammatory protein-1α receptors are present on cells enriched for CD34 expression from patients with chronic myeloid leukemia. In: Blood. 1995 ; Vol. 86, No. 11. pp. 4270-4277.
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abstract = "The response of normal and chronic myeloid leukemia (CML), CD34+cells to human macrophage inflammatory protein-1α (MIP-1α or LD78) was assessed. In tritiated thymidine incorporation assays, stem cell factor plus granulocyte- macrophage colony-stimulating factor stimulated thymidine incorporation in normal CD34+cells was reduced to 72{\%} of control values in the presence of MIP-1α, whereas incorporation by CML CD34+cells exposed to the same factors was not altered. In clonogenic assays, the presence of MIP-1α gave a level of colony formation that was 71{\%} of control values for normal progenitor cells, whereas for CML CD34+cells colony formation was enhanced by 25{\%}. These results suggest that, in vitro, CML progenitor cells are relatively refractory to the growth inhibitory effects of MIP-1α. Using flow cytometry, the specific binding of a biotinylated human MIP-1α/avidin fluorescein (FITC) conjugate to normal and CML mononuclear and CD34+cell populations was quantified. The data indicate that (for both normal and CML CD34+cells) there was a single population of cells that express cell surface receptors for MIP-1α and this receptor expression was independent of cell cycle status. CML progenitor cells may be refractory to the effects of MIP-1α as a result of events downstream from receptor expression.",
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Macrophage inflammatory protein-1α receptors are present on cells enriched for CD34 expression from patients with chronic myeloid leukemia. / Chasty, Richard C.; Lucas, Guy S.; Owen-Lynch, P. Jane; Pierce, Andrew; Whetton, Anthony D.

In: Blood, Vol. 86, No. 11, 01.12.1995, p. 4270-4277.

Research output: Contribution to journalArticle

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