ATP Synthase C-Subunit-Deficient Mitochondria Have a Small Cyclosporine A-Sensitive Channel, but Lack the Permeability Transition Pore.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
02 01 2019
Historique:
received: 24 04 2018
revised: 01 08 2018
accepted: 06 12 2018
entrez: 4 1 2019
pubmed: 4 1 2019
medline: 20 3 2020
Statut: ppublish

Résumé

Permeability transition (PT) is an increase in mitochondrial inner membrane permeability that can lead to a disruption of mitochondrial function and cell death. PT is responsible for tissue damage in stroke and myocardial infarction. It is caused by the opening of a large conductance (∼1.5 nS) channel, the mitochondrial PT pore (mPTP). We directly tested the role of the c-subunit of ATP synthase in mPTP formation by measuring channel activity in c-subunit knockout mitochondria. We found that the classic mPTP conductance was lacking in c-subunit knockout mitochondria, but channels sensitive to the PT inhibitor cyclosporine A could be recorded. These channels had a significantly lower conductance compared with the cyclosporine A-sensitive channels detected in parental cells and were sensitive to the ATP/ADP translocase inhibitor bongkrekic acid. We propose that, in the absence of the c-subunit, mPTP cannot be formed, and a distinct cyclosporine A-sensitive low-conductance channel emerges.

Identifiants

pubmed: 30605668
pii: S2211-1247(18)31963-6
doi: 10.1016/j.celrep.2018.12.033
pmc: PMC6521848
mid: NIHMS1517817
pii:
doi:

Substances chimiques

Mitochondrial Membrane Transport Proteins 0
Mitochondrial Permeability Transition Pore 0
Cyclosporine 83HN0GTJ6D
Adenosine Triphosphate 8L70Q75FXE

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

11-17.e2

Subventions

Organisme : NIA NIH HHS
ID : K01 AG054734
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM115570
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS081746
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS045876
Pays : United States
Organisme : NINDS NIH HHS
ID : R37 NS045876
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.

Références

Biochem Biophys Res Commun. 1991 May 15;176(3):1183-8
pubmed: 1710110
Proc Natl Acad Sci U S A. 2014 Jul 22;111(29):10580-5
pubmed: 24979777
Cell Cycle. 2013 Feb 15;12(4):674-83
pubmed: 23343770
Proc Natl Acad Sci U S A. 2017 Aug 22;114(34):9086-9091
pubmed: 28784775
Front Physiol. 2018 Nov 01;9:1543
pubmed: 30443222
Biochim Biophys Acta. 1995 Jul 17;1241(2):139-76
pubmed: 7640294
J Cell Biol. 2001 Nov 26;155(5):725-31
pubmed: 11724814
Proc Natl Acad Sci U S A. 2017 Mar 28;114(13):3409-3414
pubmed: 28289229
Pharmacol Res. 2015 Sep;99:382-92
pubmed: 25956324
Biochim Biophys Acta. 1998 Aug 10;1366(1-2):177-96
pubmed: 9714796
EMBO Rep. 2017 Jul;18(7):1077-1089
pubmed: 28566520
Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):5887-92
pubmed: 23530243
Cell Calcium. 2003 Feb;33(2):101-12
pubmed: 12531186
J Bioenerg Biomembr. 1992 Feb;24(1):111-7
pubmed: 1380498
Biochem J. 1990 May 15;268(1):153-60
pubmed: 2160810
J Bioenerg Biomembr. 1996 Apr;28(2):115-23
pubmed: 9132409
Mol Cell. 2015 Oct 1;60(1):47-62
pubmed: 26387735
J Bioenerg Biomembr. 1992 Feb;24(1):99-110
pubmed: 1380510
Int Rev Cytol. 2004;238:227-74
pubmed: 15364200
J Biol Chem. 1991 Feb 25;266(6):3376-9
pubmed: 1847371
Circ Res. 2015 May 22;116(11):1850-62
pubmed: 25999424
J Bioenerg Biomembr. 1989 Aug;21(4):497-506
pubmed: 2478535
Biochemistry. 1996 Jul 2;35(26):8483-8
pubmed: 8679608
Cell Physiol Biochem. 2018;50(5):1840-1855
pubmed: 30423558
Biophys J. 2005 Apr;88(4):2614-25
pubmed: 15695627
J Biol Chem. 2014 Jun 6;289(23):15980-5
pubmed: 24790105
FEBS J. 2006 May;273(10):2077-99
pubmed: 16649987
Cell Death Discov. 2016 Dec 05;2:16070
pubmed: 27924223

Auteurs

Maria A Neginskaya (MA)

College of Dentistry, Department of Basic Sciences, New York University, New York, NY 10010, USA; Laboratory of Molecular Neurobiology, Sothern Federal University, Academy of Biology and Biotechnology, 344090 Rostov-on-Don, Russia.

Maria E Solesio (ME)

College of Dentistry, Department of Basic Sciences, New York University, New York, NY 10010, USA.

Elena V Berezhnaya (EV)

College of Dentistry, Department of Basic Sciences, New York University, New York, NY 10010, USA; Laboratory of Molecular Neurobiology, Sothern Federal University, Academy of Biology and Biotechnology, 344090 Rostov-on-Don, Russia.

Giuseppe F Amodeo (GF)

College of Dentistry, Department of Basic Sciences, New York University, New York, NY 10010, USA.

Nelli Mnatsakanyan (N)

Section of Endocrinology, Department of Internal Medicine, Yale University, New Haven, CT 06511, USA.

Elizabeth A Jonas (EA)

Section of Endocrinology, Department of Internal Medicine, Yale University, New Haven, CT 06511, USA.

Evgeny V Pavlov (EV)

College of Dentistry, Department of Basic Sciences, New York University, New York, NY 10010, USA. Electronic address: ep37@nyu.edu.

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