Necrostatin-1 reverts shikonin-induced necroptosis to apoptosis

被引：223

作者：

Han, Weidong ^{[1
,2
]}

Xie, Jiansheng ^{[1
]}

Li, Ling ^{[1
]}

Liu, Zhen ^{[1
]}

Hu, Xun ^{[1
]}

机构：

[1] Zhejiang Univ, Inst Canc, Key Lab Canc Prevent & Intervent,Affiliated Hosp, Natl Minist Educ,Prov Key Lab Mol Biol Med Sci, Hangzhou 310009, Zhejiang, Peoples R China

[2] Zhejiang Univ, Sch Med, Dept Med Oncol, Sir Run Run Shaw Hosp, Hangzhou 310016, Zhejiang, Peoples R China

来源：

APOPTOSIS | 2009年 / 14卷 / 05期

关键词：

Necroptosis; Necrostatin-1; Apoptosis; Shikonin; PERMEABILITY TRANSITION PORE; MITOCHONDRIAL-MEMBRANE PERMEABILIZATION; CELL-DEATH; BCL2; FAMILY; BAX; TRANSLOCATION; RESISTANCE; INHIBITORS; COMPONENT; PROTECTS;

D O I：

10.1007/s10495-009-0334-x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Degterev et al. previously demonstrated that death receptor mediated apoptosis could be diverted to necroptosis when apoptosis signaling was blocked, suggesting that necroptosis may function as a backup mechanism to insure the elimination of damaged cells under certain conditions when apoptosis was inhibited. Here, we show that shikonin-induced necroptosis can be reverted to apoptosis in the presence of necrostatin-1 (Nec-1), a specific necroptosis inhibitor and that the death mode switch is at least partially due to the conversion from mitochondrial inner membrane permeability to mitochondrial outer membrane permeability, which is associated with Bax translocation. The data combined with the previous reports support a notion that apoptosis and necroptosis may function as reciprocal backup mechanisms of cellular demise. To the best of our knowledge, this is the first study to document a conversion from necroptosis to apoptosis.

引用

页码：674 / 686

页数：13

共 30 条

[1]

How do Bax and Bak lead to permeabilization of the outer mitochondrial membrane? [J].