Effect of CCL23/myeloid progenitor inhibitory factor 1 (MPIF-1) on the proliferation, apoptosis and differentiation of U937 cells.
- Author:
Qing GONG
1
;
Jin-E ZHENG
;
Wei LIU
;
Li-Qiong LIU
;
Yue-Ying LI
;
Shi-Ang HUANG
Author Information
1. Center for Stem Cell Research and Application, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
physiology;
Cell Proliferation;
drug effects;
Cell Transformation, Neoplastic;
drug effects;
Chemokines, CC;
pharmacology;
Humans;
U937 Cells
- From:
Journal of Experimental Hematology
2007;15(3):496-500
- CountryChina
- Language:Chinese
-
Abstract:
CCL23 is a human CC chemokine with potential suppression effects on both human and murine myeloid progenitor cells both in vitro and in vivo, and only expressed and released by dendritic cells differentiated from monocytes in blood cells. However, recent study has shown that CCL23 was over-expressed in bone marrow and peripheral blood cells from pediatric patients with acute myeloid leukemia (AML). In order to investigate the effects of CCL23 on the development, therapy and prognosis of leukemia, the U937 cells, a leukemic cell strain, were adopted and cultured with rhCCL23 for 72 hours. The cell proliferation and apoptosis rate were detected by Cell Counting Kit-8 and FITC-AnnexinV/PI respectively; the morphologic changes and the expression of CCR1 (the only receptor of CCL23 known by now) were observed during the differentiation process. The results showed that no obvious effect on the proliferation, apoptosis and differentiation of U937 was found by using CCL23 alone (P > 0.05), but cultured in combination with CCL23 and PMA, the differentiation of U937 cells were promoted remarkably, during which the CCR1 expression increased (P < 0.05). It is concluded that CCL23 alone did not inhibit the proliferation and differentiation of U937, while its use in combination with PMA may possess synergistic effect on inducting differentiation of U937 through the increase of receptor CCR1 expression.
