Effect of GPI-PLD on adhesion function of bone marrow mononuclear cell from patients with myeloid leukemia and its mechanism.
- Author:
Guang-Fen XIAO
1
;
Fang-Ping CHEN
;
Bin FU
;
Guang-Pin WANG
;
Zai-Fu JIAN
Author Information
1. Department of Hematology, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Adolescent;
Adult;
Aged;
Bone Marrow Cells;
drug effects;
metabolism;
pathology;
CD24 Antigen;
biosynthesis;
Cell Adhesion;
drug effects;
Cell Survival;
drug effects;
Child;
Female;
Humans;
Immunohistochemistry;
Leukemia, Myeloid;
blood;
Leukocytes, Mononuclear;
drug effects;
metabolism;
pathology;
Male;
Middle Aged;
Phenanthrolines;
pharmacology;
Phospholipase D;
blood;
metabolism
- From:
Journal of Experimental Hematology
2005;13(3):369-372
- CountryChina
- Language:Chinese
-
Abstract:
To explore the effect of glycosyl-phosphatidyl inositol-specific phospholipase D (GPI-PLD) on the adhesion function of bone marrow mononuclear cell from patients with myeloid leukemia and analyze its mechanism, the activity of GPI-PLD in bone marrow mononuclear cell from the patients were measured by using GPI-anchored placental alkaline phosphatase (PLAP) as substrate and Triton-X114 partitioning; the adhesion rate and CD24 expression of these cells were measured by MTT and immunohistochemical method respectively, when these cells were or were not treated by 1 mmol/L 1,10-phenanthroline for 5 hours. The results showed that the GPI-PLD activity of bone marrow mononuclear cells from the patients was significantly inhibited after being treated by 1 mmol/L 1, 10-phenanthroline for 5 hours [(42.08 +/- 7.21)% vs (5.4 +/- 2.96)%], while the adhesion rate and the expression of CD24 of these cells were increased [(49.78 +/- 26.73)% vs (61.19 +/- 29.14)%, (16.02 +/- 9.68)% vs (18.5 +/- 11.14)%, respectively)]. It is concluded that depression of GPI-PLD activity can increase the adhesion rate of bone marrow mononuclear cells from the patients while the CD24 expression is enhanced.
