Involvement of receptor aggregation and reactive oxygen species in osmotic stress-induced Syk activation in B cells

被引:20
作者
Qin, SF [1 ]
Ding, JY [1 ]
Takano, T [1 ]
Yamamura, H [1 ]
机构
[1] Kobe Univ, Sch Med, Dept Biochem, Chuo Ku, Kobe, Hyogo 6500017, Japan
关键词
osmotic stress; reactive oxygen species; protein-tyrosine kinase; Syk;
D O I
10.1006/bbrc.1999.1079
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Syk has been shown to be activated by osmotic stress, however, the mechanisms involved are largely unknown. In this study, we demonstrated that cell shrinkage, rather than osmolarity, was responsible for osmotic stress-induced Syk activation. Osmotic stress-induced Syk activation depended partly upon aggregation of surface receptors. Moreover, intracellular reactive oxygen species were involved in mediating osmotic stress-induced Syk activation, with osmotic stress-induced Syk activation being inhibited by the pretreatment of cells with N-acetyl-cysteine and reduced glutathione. When cells were treated with the combination of sodium chloride and hydrogen peroxide, there was a synergistic activation of Syk. In conclusion, osmotic stress-induced Syk activation required suramin-inhibitable surface receptor aggregation and accumulation of intracellular reactive oxygen species. (C) 1999 Academic Press.
引用
收藏
页码:231 / 236
页数:6
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