beta1 Integrin Dysfunction in Adult Chronic Myeloid Leukemia Bone Marrow Cells
- Author:
Renkui BAI
1
;
Shanshan CHEN
;
Yanrong LIU
;
Jiayu FU
;
Jinlan LI
;
Hong YU
;
Yan CHANG
;
Guori RUAN
Author Information
1. Institute of Hematology and People's Hospital, Beijing Medical University, Beijing 100034, China.
- Publication Type:Journal Article
- From:
Journal of Experimental Hematology
2000;8(2):85-89
- CountryChina
- Language:Chinese
-
Abstract:
According to our previous experiments, Ph(+) chronic myeloid leukemia (CML) cell line K562 cells have defects in beta 1 integrin activation. In order to search the same regularity in Ph(+) CML bone marrow cells, bone marrow mononuclear cells (BMMNC) from 12 cases of Ph(+) CML and 10 cases of normal individuals were studied. Their expression rate of 9EG7 epitope on beta1 integrin post treatment by 8A2 or GM- or G-CSF and cell adhesion ability with soluble fibronectin (FN) were evaluated by flow cytometry; in addition, the effects of CGP57148B, a highly specific ABL tyrosine kinase inhibitor, were observed. Our results showed that 9EG7 expression rate and FN binding rate were very low in all the inactivated cells. The parameter increased markedly post 8A2 activation in both NBMMNCs and CMLBMMNCs, but the degree of increase in CMLBMMNCs was significantly lower than that in NBMMNCs; GM-CSF or G-CSF could significantly increase the parameters in NBMMNCs while had no effects on that in CMLBMMNCs. CGP57148B could increase the beta1 integrin activation potential of CMLBMMNCs but had no effects on that of NBMMNCs. The results indicate that decreased activation potential of beta1 integrin in CMLBMMNCs is the major cause of adhesion defects of Ph(+) CML cells; beta1 integrin functional insufficiency in CMLBMMNCs could not be directly reversed by ABL tyrosine kinase inhibitor CGP57148B.
