Bcl-2 blocks loss of mitochondrial membrane potential while ICE inhibitors act at a different step during inhibition of death induced by respiratory chain inhibitors
- PMID: 8700549
Bcl-2 blocks loss of mitochondrial membrane potential while ICE inhibitors act at a different step during inhibition of death induced by respiratory chain inhibitors
Abstract
Bcl-2, Bcl-xL, CrmA and tetrapeptide ICE inhibitor reduce the extent of necrotic cell death induced by cyanide, which primarily damages mitochondria. Although none of them affects the drastic decrease in ATP levels induced by cyanide, Bcl-2 and Bcl-xL but not CrmA or ICE inhibitor inhibit the cyanide-induced decrease in mitochondrial membrane potential. A similar blocking effect is observed on necrotic cell death induced by other respiration inhibitors, rotenone and antimycin A, and on apoptotic cell death induced by etoposide or calcium ionophore. These results indicate that Bc1-2 and Bcl-xL protect mitochondria against the loss of function during both apoptosis and at least some forms of necrotic cell death. The ICE family proteases act at a different step other than the loss of mitochondrial membrane potential.
Similar articles
-
Retardation of chemical hypoxia-induced necrotic cell death by Bcl-2 and ICE inhibitors: possible involvement of common mediators in apoptotic and necrotic signal transductions.Oncogene. 1996 May 16;12(10):2045-50. Oncogene. 1996. PMID: 8668329
-
Mitochondrial membrane permeabilization is a critical step of lysosome-initiated apoptosis induced by hydroxychloroquine.Oncogene. 2003 Jun 19;22(25):3927-36. doi: 10.1038/sj.onc.1206622. Oncogene. 2003. PMID: 12813466
-
Bcl-2 and Bcl-xL block apoptosis as well as necrosis: possible involvement of common mediators in apoptotic and necrotic signal transduction pathways.Leukemia. 1997 Apr;11 Suppl 3:380-2. Leukemia. 1997. PMID: 9209397
-
Mechanisms of cell death in hypoxia/reoxygenation injury.Oncogene. 1998 Dec 24;17(25):3341-9. doi: 10.1038/sj.onc.1202579. Oncogene. 1998. PMID: 9916996 Review.
-
The Bcl-xL and Bax-alpha control points: modulation of apoptosis induced by cancer chemotherapy and relation to TPCK-sensitive protease and caspase activation.Biochem Cell Biol. 1997;75(4):301-14. Biochem Cell Biol. 1997. PMID: 9493953 Review.
Cited by
-
The role of receptor internalization in CD95 signaling.EMBO J. 2006 Mar 8;25(5):1009-23. doi: 10.1038/sj.emboj.7601016. Epub 2006 Feb 23. EMBO J. 2006. PMID: 16498403 Free PMC article.
-
The permeability transition pore complex: a target for apoptosis regulation by caspases and bcl-2-related proteins.J Exp Med. 1998 Apr 20;187(8):1261-71. doi: 10.1084/jem.187.8.1261. J Exp Med. 1998. PMID: 9547337 Free PMC article.
-
The rasGAP-binding protein, Dok-1, mediates activin signaling via serine/threonine kinase receptors.EMBO J. 2002 Apr 2;21(7):1684-94. doi: 10.1093/emboj/21.7.1684. EMBO J. 2002. PMID: 11927552 Free PMC article.
-
Regulation of macrophage gene expression by Mycobacterium tuberculosis: down-regulation of mitochondrial cytochrome c oxidase.Infect Immun. 1998 Aug;66(8):3952-8. doi: 10.1128/IAI.66.8.3952-3958.1998. Infect Immun. 1998. PMID: 9673285 Free PMC article.
-
Persea declinata (Bl.) Kosterm Bark Crude Extract Induces Apoptosis in MCF-7 Cells via G0/G1 Cell Cycle Arrest, Bcl-2/Bax/Bcl-xl Signaling Pathways, and ROS Generation.Evid Based Complement Alternat Med. 2014;2014:248103. doi: 10.1155/2014/248103. Epub 2014 Apr 7. Evid Based Complement Alternat Med. 2014. PMID: 24808916 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Research Materials