Small-Molecule Inhibitors of Cyclophilins Block Opening of the Mitochondrial Permeability Transition Pore and Protect Mice From Hepatic Ischemia/Reperfusion Injury.


Journal

Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630

Informations de publication

Date de publication:
11 2019
Historique:
received: 23 07 2018
revised: 12 07 2019
accepted: 16 07 2019
pubmed: 25 7 2019
medline: 20 12 2019
entrez: 24 7 2019
Statut: ppublish

Résumé

Hepatic ischemia/reperfusion injury is a complication of liver surgery that involves mitochondrial dysfunction resulting from mitochondrial permeability transition pore (mPTP) opening. Cyclophilin D (PPIF or CypD) is a peptidyl-prolyl cis-trans isomerase that regulates mPTP opening in the inner mitochondrial membrane. We investigated whether and how recently created small-molecule inhibitors of CypD prevent opening of the mPTP in hepatocytes and the resulting effects in cell models and livers of mice undergoing ischemia/reperfusion injury. We measured the activity of 9 small-molecule inhibitors of cyclophilins in an assay of CypD activity. The effects of the small-molecule CypD inhibitors or vehicle on mPTP opening were assessed by measuring mitochondrial swelling and calcium retention in isolated liver mitochondria from C57BL/6J (wild-type) and Ppif The compounds inhibited peptidyl-prolyl isomerase activity (half maximal inhibitory concentration values, 0.2-16.2 μmol/L) and, as a result, calcium-induced mitochondrial swelling, by preventing mPTP opening (half maximal inhibitory concentration values, 1.4-132 μmol/L) in a concentration-dependent manner. The most potent inhibitor (C31) bound CypD with high affinity and inhibited swelling in mitochondria from livers of wild-type and Ppif Recently created small-molecule inhibitors of CypD reduced calcium-induced swelling in mitochondria from mouse and human liver tissues. Administration of these compounds to mice during ischemia/reperfusion restored hepatic calcium retention capacity and oxidative phosphorylation parameters and reduced liver damage. These compounds might be developed to protect patients from ischemia/reperfusion injury after liver surgery or for other hepatic or nonhepatic disorders related to abnormal mPTP opening.

Sections du résumé

BACKGROUND & AIMS
Hepatic ischemia/reperfusion injury is a complication of liver surgery that involves mitochondrial dysfunction resulting from mitochondrial permeability transition pore (mPTP) opening. Cyclophilin D (PPIF or CypD) is a peptidyl-prolyl cis-trans isomerase that regulates mPTP opening in the inner mitochondrial membrane. We investigated whether and how recently created small-molecule inhibitors of CypD prevent opening of the mPTP in hepatocytes and the resulting effects in cell models and livers of mice undergoing ischemia/reperfusion injury.
METHODS
We measured the activity of 9 small-molecule inhibitors of cyclophilins in an assay of CypD activity. The effects of the small-molecule CypD inhibitors or vehicle on mPTP opening were assessed by measuring mitochondrial swelling and calcium retention in isolated liver mitochondria from C57BL/6J (wild-type) and Ppif
RESULTS
The compounds inhibited peptidyl-prolyl isomerase activity (half maximal inhibitory concentration values, 0.2-16.2 μmol/L) and, as a result, calcium-induced mitochondrial swelling, by preventing mPTP opening (half maximal inhibitory concentration values, 1.4-132 μmol/L) in a concentration-dependent manner. The most potent inhibitor (C31) bound CypD with high affinity and inhibited swelling in mitochondria from livers of wild-type and Ppif
CONCLUSIONS
Recently created small-molecule inhibitors of CypD reduced calcium-induced swelling in mitochondria from mouse and human liver tissues. Administration of these compounds to mice during ischemia/reperfusion restored hepatic calcium retention capacity and oxidative phosphorylation parameters and reduced liver damage. These compounds might be developed to protect patients from ischemia/reperfusion injury after liver surgery or for other hepatic or nonhepatic disorders related to abnormal mPTP opening.

Identifiants

pubmed: 31336123
pii: S0016-5085(19)41119-0
doi: 10.1053/j.gastro.2019.07.026
pii:
doi:

Substances chimiques

Peptidyl-Prolyl Isomerase F 0
Enzyme Inhibitors 0
Mitochondrial Membrane Transport Proteins 0
Mitochondrial Permeability Transition Pore 0
PPIF protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1368-1382

Informations de copyright

Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.

Auteurs

Mathieu Panel (M)

INSERM U955, Team 3, Créteil, France; Université Paris-Est, UMR S955, DHU A-TVB, UPEC, Créteil, France.

Isaac Ruiz (I)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France.

Rozenn Brillet (R)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France.

Fouad Lafdil (F)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France; Institut Universitaire de France (IUF), Paris, France.

Fatima Teixeira-Clerc (F)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France.

Cong Trung Nguyen (CT)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France; Department of Pathology, Hôpital Henri Mondor, Université Paris-Est, Créteil, France.

Julien Calderaro (J)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France; Department of Pathology, Hôpital Henri Mondor, Université Paris-Est, Créteil, France.

Muriel Gelin (M)

Centre de Biochimie Structurale (CBS), INSERM U1054, CNRS UMR5048, Université de Montpellier, Montpellier, France.

Fred Allemand (F)

Centre de Biochimie Structurale (CBS), INSERM U1054, CNRS UMR5048, Université de Montpellier, Montpellier, France.

Jean-François Guichou (JF)

Centre de Biochimie Structurale (CBS), INSERM U1054, CNRS UMR5048, Université de Montpellier, Montpellier, France.

Bijan Ghaleh (B)

INSERM U955, Team 3, Créteil, France; Université Paris-Est, UMR S955, DHU A-TVB, UPEC, Créteil, France.

Abdelhakim Ahmed-Belkacem (A)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France.

Didier Morin (D)

INSERM U955, Team 3, Créteil, France; Université Paris-Est, UMR S955, DHU A-TVB, UPEC, Créteil, France. Electronic address: didier.morin@inserm.fr.

Jean-Michel Pawlotsky (JM)

INSERM U955, Team Viruses, Hepatology, Cancer, Créteil, France; National Reference Center for Viral Hepatitis B, C and Delta, Department of Virology, Hôpital Henri Mondor, Université Paris-Est, Créteil, France. Electronic address: jean-michel.pawlotsky@aphp.fr.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH