CKbeta8-1 alters expression of cyclin E in colony forming units-granulocyte macrophage (CFU-GM) lineage from human cord blood CD34 + cells.
- Author:
Eui Kyu NOH
1
;
Jae Sun RA
;
Seong Ae LEE
;
Byoung S KWON
;
In Seob HAN
Author Information
1. Immunomodulation Research Center, Department of Biological Science, University of Ulsan, Ulsan 680-749, Korea. hanis@ulsan.ac.kr
- Publication Type:Case Report ; Research Support, Non-U.S. Gov't
- Keywords:
cell cycle;
chemokine;
cyclin E;
granulocytes;
macrophages;
multi potent;
stem cells
- MeSH:
Antigens, CD34/metabolism;
Cell Cycle Proteins/metabolism;
Cell Lineage;
Cells, Cultured;
Chemokines, CC/*pharmacology;
Cyclin E/*metabolism;
Fetal Blood/*cytology;
G1 Phase/drug effects;
Gene Expression Regulation/*drug effects;
Granulocytes/cytology/*drug effects/metabolism;
Growth Substances/pharmacology;
Humans;
Macrophages/cytology/*drug effects/metabolism;
Research Support, Non-U.S. Gov't;
Stem Cells/cytology/*drug effects/metabolism
- From:Experimental & Molecular Medicine
2005;37(6):619-623
- CountryRepublic of Korea
- Language:English
-
Abstract:
A C6 beta-chemokine, CKbeta8-1, suppressed the colony formation of CD34 + cells of human cord blood (CB). Molecular mechanisms involved in CKbeta8-1-medicated suppression of colony formation of CD34 + cells are not known. To address this issue, the level of various G1/S cell cycle regulating proteins in CKbeta8-1-treated CD34 + cells were compared with those in untreated CD34 + cells. CKbeta8-1 did not significantly alter the expression of the G1/S cycle regulation proteins (cyclin D1, D3, and E), CDK inhibitor (p27and Rb), and other cell proliferation regulation protein (p53) in CB CD34 + cells. Here we describe an in vitro system in which CB CD34 + cells were committed to a multipotent progenitor lineage of colony forming units-granulocyte/macrophage (CFU-GM) by a simple combination of recombinant human (rh) GM-CSF and rhIL-3. In this culture system, we found that cyclin E protein appeared later and disappeared faster in the CKbeta8-1-treated cells than in the control cells during CFU-GM lineage development. These findings suggested that cyclin E may play a role in suppressing the colony formation of CFU-GM by CKbeta8-1.