Arsenic trioxide induces endoplasmic reticulum stress-related events in neutrophils

被引:33
作者
Binet, Francois [1 ]
Chiasson, Sonia [1 ]
Girard, Denis [1 ]
机构
[1] Univ Quebec, Inst Armand Frappier, INRS, Lab Rech Inflammat & Physiol Granulocytes, Laval, PQ, Canada
基金
加拿大自然科学与工程研究理事会; 加拿大健康研究院;
关键词
Arsenic trioxide; Neutrophils; Apoptosis; Ubiquitination; Calcium; Caspases; ACUTE PROMYELOCYTIC LEUKEMIA; NOVO PROTEIN-SYNTHESIS; INDUCED APOPTOSIS; ER STRESS; INVOLVEMENT; CASPASE-12; CELLS; ACTIVATION; INFLAMMATION; CALCINEURIN;
D O I
10.1016/j.intimp.2010.01.013
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We recently reported that the endoplasmic reticulum (ER)-induced cell pathway of apoptosis is operational in human neutrophils and that some ER stressors can accelerate this process. Recent data suggest that arsenic trioxide (As2O3 or AID), may also act as an ER stressor. The aims of the present study were to elucidate if other ER stress-related events occur in ATO-induced neutrophils, and to determine the role of caspase-4 in the proapoptotic activity of ATO. We found that ATO induced ubiquitination of proteins, and increased calcium concentration and gene expression of calcineurin in neutrophils. In addition to caspase-4, activities of caspase-3, -8 and -9 were increased by AID. The processing of caspase-4 was reversed by a caspase-8 inhibitor, indicating that caspase-4 activation requires the action of upstream initiator components, questioning on the role of caspase-4 in ATO-induced ER stress-mediated cell apoptosis. Using caspase-4 deficient THP-1 cells, we demonstrated that the proapoptotic effect of ATO was similar to that of control caspase-4-positive cells. We conclude that ATO is an ER stressor that can induce cell apoptosis by a mechanism which does not require caspase-4. In addition, we conclude that caspase-4 activation in ATO-induced neutrophils could be involved in functions other than apoptosis. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:508 / 512
页数:5
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