TRAIL causes cleavage of bid by caspase-8 and loss of mitochondrial membrane potential resulting in apoptosis in BJAB cells

被引:117
作者
Yamada, H
Tada-Oikawa, S
Uchida, A
Kawanishi, S [1 ]
机构
[1] Mie Univ, Sch Med, Dept Hyg, Tsu, Mie 5148507, Japan
[2] Mie Univ, Sch Med, Dept Orthopaed Surg, Tsu, Mie 5148507, Japan
关键词
D O I
10.1006/bbrc.1999.1641
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
A new member of the TNF family, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), has been shown to induce apoptosis. However, the mechanism for TRAIL-induced apoptosis remains to be clarified. SDS-PAGE and Western blot analysis showed that cleavage of Bid was induced by a 1-h incubation of BJAB cells with TRAIL and was blocked by a caspase-8 inhibitor. Flow cytometry demonstrated that loss of mitochondrial membrane potential in BJAB cells began about 1.5 h after the treatment with TRAIL and was apparent at 2 h in comparison with the control. DNA ladder formation, which is characteristic for apoptosis, in the cells treated with TRAIL was detected at 2 h and observed most effectively at 3 h. The time course study suggests that TRAIL causes cleavage of Bid via activation of caspase-8, subsequently the loss of mitochondrial membrane potential, resulting in apoptosis in BJAB cells. (C) 1999 Academic Press.
引用
收藏
页码:130 / 133
页数:4
相关论文
共 32 条
[1]   Human ICE/CED-3 protease nomenclature [J].
Alnemri, ES ;
Livingston, DJ ;
Nicholson, DW ;
Salvesen, G ;
Thornberry, NA ;
Wong, WW ;
Yuan, JY .
CELL, 1996, 87 (02) :171-171
[2]   Death receptors: Signaling and modulation [J].
Ashkenazi, A ;
Dixit, VM .
SCIENCE, 1998, 281 (5381) :1305-1308
[3]   Apoptosis induced by microinjection of cytochrome c is caspase-dependent and is inhibited by Bcl-2 [J].
Brustugun, OT ;
Fladmark, KE ;
Doskeland, SO ;
Orrenius, S ;
Zhivotovsky, B .
CELL DEATH AND DIFFERENTIATION, 1998, 5 (08) :660-668
[4]   Solution structure of BID, an intracellular amplifier of apoptotic signaling [J].
Chou, JJ ;
Li, HL ;
Salvesen, GS ;
Yuan, JY ;
Wagner, G .
CELL, 1999, 96 (05) :615-624
[5]   A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD [J].
Enari, M ;
Sakahira, H ;
Yokoyama, H ;
Okawa, K ;
Iwamatsu, A ;
Nagata, S .
NATURE, 1998, 391 (6662) :43-50
[6]  
Griffith TS, 1998, J IMMUNOL, V161, P2833
[7]   Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death [J].
Gross, A ;
Yin, XM ;
Wang, K ;
Wei, MC ;
Jockel, J ;
Millman, C ;
Erdjument-Bromage, H ;
Tempst, P ;
Korsmeyer, SJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (02) :1156-1163
[8]   Redox regulation of the caspases during apoptosis [J].
Hampton, MB ;
Fadeel, B ;
Orrenius, S .
TOWARDS PROLONGATION OF THE HEALTHY LIFE SPAN: PRACTICAL APPROACHES TO INTERVENTION, 1998, 854 :328-335
[9]  
HOGLIN L, 1998, CELL, V94, P491
[10]   The CED-4-homologous protein FLASH is involved in Fas-mediated activation of caspase-8 during apoptosis [J].
Imai, Y ;
Kimura, T ;
Murakami, A ;
Yajima, N ;
Sakamaki, K ;
Yonehara, S .
NATURE, 1999, 398 (6730) :777-785