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.
Affiliation
CRC Section of Haemopoietic Cell and Gene Therapeutics, Paterson Institute for Cancer Research, Manchester, United Kingdom.Issue Date
1998
Metadata
Show full item recordAbstract
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.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 CellsJournal
Stem CellsDOI
10.1002/stem.160349PubMed ID
9766815Type
ArticleLanguage
enISSN
1066-5099ae974a485f413a2113503eed53cd6c53
10.1002/stem.160349
Scopus Count
Collections
Related articles
- MIP-1alpha and TGF-beta production in CD34+ progenitor-stromal cell coculture systems: effects of progenitor isolation method and cell-cell contact.
- Authors: Liesveld JL, Harbol AW, Belanger T, Rosell KE, Abboud CN
- Issue date: 2000 Aug
- Differential effects of the hematopoietic inhibitors MIP-1 alpha, TGF-beta, and TNF-alpha on cytokine-induced proliferation of subpopulations of CD34+ cells purified from cord blood and fetal liver.
- Authors: Mayani H, Little MT, Dragowska W, Thornbury G, Lansdorp PM
- Issue date: 1995 May
- CCR1 chemokine receptor expression isolates erythroid from granulocyte-macrophage progenitors.
- Authors: de Wynter EA, Heyworth CM, Mukaida N, Jaworska E, Weffort-Santos A, Matushima K, Testa NG
- Issue date: 2001 Sep
- CD34++ CD38- and CD34+ CD38+ human hematopoietic progenitors from fetal liver, cord blood, and adult bone marrow respond differently to hematopoietic cytokines depending on the ontogenic source.
- Authors: Weekx SF, Van Bockstaele DR, Plum J, Moulijn A, Rodrigus I, Lardon F, De Smedt M, Nijs G, Lenjou M, Loquet P, Berneman ZN, Snoeck HW
- Issue date: 1998 Oct
- MIP-1alpha utilizes both CCR1 and CCR5 to induce osteoclast formation and increase adhesion of myeloma cells to marrow stromal cells.
- Authors: Oba Y, Lee JW, Ehrlich LA, Chung HY, Jelinek DF, Callander NS, Horuk R, Choi SJ, Roodman GD
- Issue date: 2005 Mar