GM-CSF AND PHORBOL ESTERS MODULATE GM-CSF RECEPTOR EXPRESSION BY INDEPENDENT MECHANISMS

被引:7
作者
BRIZZI, MF
ARDUINO, C
AVANZI, GC
BUSSOLINO, F
PEGORARO, L
机构
[1] UNIV TURIN,DIPARTIMENTO GENET BIOL & CHIM MED,I-10126 TURIN,ITALY
[2] UNIV TURIN,IST FARMACOL & TERAPIA SPERIMENTALE,I-10126 TURIN,ITALY
关键词
D O I
10.1002/jcp.1041480104
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Human granulocyte-macrophage colony-stimulating factor (GM-CSF) (0.1 nM) down-modulates its receptor in IL-3/GM-CSF dependent M-07e cells, in KG-1 cells and normal granulocytes, whereas phorbol esters 12-O-tetradecanoylphorbol-13-acetate (TPA) (2 nM) down-modulates the GM-CSF receptor in M-07e cells and granulocytes but not in KG-1 cells. As data analysis shows by nonlinear regression, the decreased binding ability depends on a reduction of the binding sites with no significant change of their dissociation constant. To gain insight into the mechanisms involved in the GM-CSF receptor regulation, we investigated the role of protein kinase C (PKC). GM-CSF, unlike TPA, was unable to activate PKC in all the cells studied. Moreover, unlike TPA, GM-CSF was still able to down-modulate its receptor in cells where PKC was inhibited by 1-(5-isoquinolonesulphonyl)-2-methylpiperazine (H7) and staurosporine or in cells where PKC was exhausted by prolonged incubation with 1-mu-M TPA. Finally, the receptor re-expression rate was accelerated by protein kinases inhibitors. These results, taken together, indicate the presence of a PKC-dependent and -independent down-modulation mechanism and a negative role of the endogeneous protein kinases in GM-CSF receptor re-expression.
引用
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页码:24 / 34
页数:11
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