Involvement of polyamines in B cell receptor-mediated apoptosis: Spermine functions as a negative modulator

被引:35
|
作者
Nitta, T
Igarashi, K
Yamashita, A
Yamamoto, M
Yamamoto, N
机构
[1] Tokyo Med & Dent Univ, Sch Med, Dept Microbiol & Mol Virol, Bunkyo Ku, Tokyo 1138519, Japan
[2] Chiba Univ, Fac Pharmaceut Sci, Chiba 260, Japan
[3] Natl Def Med Coll, Dept Biochem 2, Tokorozawa, Saitama, Japan
关键词
apoptosis; B cell; polyamine; SAGE; spermine; WEHI231;
D O I
10.1006/excr.2001.5177
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The B cell lymphoma WEHI231 has been used as a model for studying clonal deletion of B cells on the basis of its ability to undergo growth arrest and apoptosis by B cell antigen receptor (BCR) cross-linking. To comprehensively analyze the genes involved in BCR-mediated apoptosis, we applied the technique of serial analysis of gene expression (SAGE) to WEHI231. Comparison of expression patterns revealed that BCR cross-linking caused coordinate changes in the expression of genes involved in polyamine metabolism, Polyamines are ubiquitous compounds required for cell proliferation and homeostasis. The coordinate expression of the polyamine-related genes was confirmed by semiquantitative reverse transcriptase-polymerase chain reaction analysis. During apoptosis, the genes involved in polyamine biosynthesis were downregulated, whereas those involved in polyamine catabolism were upregulated, suggesting that intracellular polyamines play a role in BCR-mediated apoptosis, Levels of intracellular putrescine, spermidine, and spermine were reduced after BCR crosslinking. These effects were prevented by concurrent CD40 stimulation, which blocked BCR-mediated apoptosis, Furthermore, addition of spermine could repress the BCR-mediated apoptosis by attenuating the mitochondrial membrane potential (Delta psim) loss and activation of caspase-7 induced by BCR signaling. These findings strongly suggest that polyamine regulation is involved in apoptosis during B cell clonal deletion. (C) 2001 Academic Press.
引用
收藏
页码:174 / 183
页数:10
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