TNF-α induced altered signaling mechanism in human neutrophil

被引：49

作者：

Das, S ^{[1
]}

Bhattacharyya, S ^{[1
]}

Ghosh, S ^{[1
]}

Majumdar, S ^{[1
]}

机构：

[1] Bose Inst, Dept Microbiol, Calcutta 700054, W Bengal, India

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 1999年 / 197卷 / 1-2期

关键词：

neutrophil; PKC; TNF-alpha; apoptosis; DNA fragmentation;

D O I：

10.1023/A:1006935114624

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

In the present study we investigated the TNF-alpha induced signal transduction mechanism in human neutrophil. Exogenously added TNF-alpha affects both PKC activity and its translocation from cytosol to the membrane. Endogenous protein phosphorylation pattern is inhibited in TNF-alpha induced neutrophil in Ca-dependent and Ca-independent manner, including a major 47 and 66 kDa cytosolic proteins, which may be implicated in superoxide anion generation. However TNF-alpha dose dependently enhances the expression of zeta-PKC isotype but not the beta-PKC. Morphology and cell cytotoxicity are studied in TNF-alpha treated neutrophil to understand the TNF-alpha induced cell death or apoptosis and these experiment is further confirmed by DNA fragmentation analysis. These results clearly demonstrate that TNF-alpha induces cellular death of human neutrophil at least in part by enhanced expression of Ca-independent zeta-PKC. These observations provide an insight towards understanding the function of zeta-PKC in apoptotic pathway.

引用

页码：97 / 108

页数：12

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