Differential response of CD34+ cells isolated from cord blood and bone marrow to MIP-1 alpha and the expression of MIP-1 alpha receptors on these immature cells.

2.50
Hdl Handle:
http://hdl.handle.net/10541/92999
Title:
Differential response of CD34+ cells isolated from cord blood and bone marrow to MIP-1 alpha and the expression of MIP-1 alpha receptors on these immature cells.
Authors:
De Wynter, Erika A; Durig, J; Cross, Michael A; Heyworth, Clare M; Testa, Nydia G
Abstract:
Macrophage inflammatory protein-1 alpha (MIP-1alpha) has been shown to have a role in the control of myeloid stem and progenitor cell proliferation. Recent evidence suggests that MIP-1alpha also has a stimulatory effect on proliferation of mature progenitors as well as an inhibitory effect on immature progenitors in vitro. We have compared the effect of MIP-1alpha on myeloid and erythroid colony formation of CD34+ cells isolated from bone marrow and cord blood. In the presence of MIP-1alpha, bone marrow granulocyte-macrophage-colony forming cells (GM-CFC) were inhibited over a dose range of 15 ng/ml to 500 ng/ml, and GM-CFC from cord blood CD34+ cells were stimulated over the same dose range. MIP-1alpha suppressed BFU-E colonies in both bone marrow and cord blood. Using thymidine suicide assays, the influence of MIP-1alpha on the cycling status of the cells was assessed. A good correlation between the effect of MIP-1alpha on colony formation and cell cycle progression was observed. These results suggest that there is a differential response to MIP-1alpha when bone marrow and cord blood CD34+ cells are compared. Using flow cytometry and a biotinylated human MIP-1alpha/avidin fluorescein conjugate, the expression of MIP-1alpha receptors on CD34+ cells was assessed. The data indicated that there was little quantitative difference in overall expression of receptors (82.9% versus 93%) from bone marrow or cord blood, respectively. However, when Northern blot analysis was used, mRNA for two different MIP-1alpha receptors CCR1 and CCR5 could be detected in bone marrow, but only CCR1 mRNA was seen in cord blood CD34+ samples. Therefore, the expression of different receptor subtypes on CD34+ cells may be responsible for the difference in MIP-1alpha responsiveness observed.
Affiliation:
CRC Section of Haemopoietic Cell and Gene Therapeutics, Paterson Institute for Cancer Research, Manchester, United Kingdom.
Citation:
Differential response of CD34+ cells isolated from cord blood and bone marrow to MIP-1 alpha and the expression of MIP-1 alpha receptors on these immature cells. 1998, 16 (5):349-56 Stem Cells
Journal:
Stem Cells
Issue Date:
1998
URI:
http://hdl.handle.net/10541/92999
DOI:
10.1002/stem.160349
PubMed ID:
9766815
Type:
Article
Language:
en
ISSN:
1066-5099
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorDe Wynter, Erika Aen
dc.contributor.authorDurig, Jen
dc.contributor.authorCross, Michael Aen
dc.contributor.authorHeyworth, Clare Men
dc.contributor.authorTesta, Nydia Gen
dc.date.accessioned2010-02-25T11:16:23Z-
dc.date.available2010-02-25T11:16:23Z-
dc.date.issued1998-
dc.identifier.citationDifferential response of CD34+ cells isolated from cord blood and bone marrow to MIP-1 alpha and the expression of MIP-1 alpha receptors on these immature cells. 1998, 16 (5):349-56 Stem Cellsen
dc.identifier.issn1066-5099-
dc.identifier.pmid9766815-
dc.identifier.doi10.1002/stem.160349-
dc.identifier.urihttp://hdl.handle.net/10541/92999-
dc.description.abstractMacrophage inflammatory protein-1 alpha (MIP-1alpha) has been shown to have a role in the control of myeloid stem and progenitor cell proliferation. Recent evidence suggests that MIP-1alpha also has a stimulatory effect on proliferation of mature progenitors as well as an inhibitory effect on immature progenitors in vitro. We have compared the effect of MIP-1alpha on myeloid and erythroid colony formation of CD34+ cells isolated from bone marrow and cord blood. In the presence of MIP-1alpha, bone marrow granulocyte-macrophage-colony forming cells (GM-CFC) were inhibited over a dose range of 15 ng/ml to 500 ng/ml, and GM-CFC from cord blood CD34+ cells were stimulated over the same dose range. MIP-1alpha suppressed BFU-E colonies in both bone marrow and cord blood. Using thymidine suicide assays, the influence of MIP-1alpha on the cycling status of the cells was assessed. A good correlation between the effect of MIP-1alpha on colony formation and cell cycle progression was observed. These results suggest that there is a differential response to MIP-1alpha when bone marrow and cord blood CD34+ cells are compared. Using flow cytometry and a biotinylated human MIP-1alpha/avidin fluorescein conjugate, the expression of MIP-1alpha receptors on CD34+ cells was assessed. The data indicated that there was little quantitative difference in overall expression of receptors (82.9% versus 93%) from bone marrow or cord blood, respectively. However, when Northern blot analysis was used, mRNA for two different MIP-1alpha receptors CCR1 and CCR5 could be detected in bone marrow, but only CCR1 mRNA was seen in cord blood CD34+ samples. Therefore, the expression of different receptor subtypes on CD34+ cells may be responsible for the difference in MIP-1alpha responsiveness observed.en
dc.language.isoenen
dc.subject.meshAntigens, CD34-
dc.subject.meshBone Marrow Cells-
dc.subject.meshCells, Cultured-
dc.subject.meshChemokine CCL3-
dc.subject.meshChemokine CCL4-
dc.subject.meshColony-Forming Units Assay-
dc.subject.meshDNA-
dc.subject.meshFetal Blood-
dc.subject.meshFlow Cytometry-
dc.subject.meshHumans-
dc.subject.meshLeukocytes, Mononuclear-
dc.subject.meshMacrophage Inflammatory Proteins-
dc.subject.meshRNA, Messenger-
dc.subject.meshReceptors, Chemokine-
dc.subject.meshStem Cells-
dc.titleDifferential response of CD34+ cells isolated from cord blood and bone marrow to MIP-1 alpha and the expression of MIP-1 alpha receptors on these immature cells.en
dc.typeArticleen
dc.contributor.departmentCRC Section of Haemopoietic Cell and Gene Therapeutics, Paterson Institute for Cancer Research, Manchester, United Kingdom.en
dc.identifier.journalStem Cellsen
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