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ToxSci Advance Access originally published online on June 11, 2008
Toxicological Sciences 2008 105(1):44-50; doi:10.1093/toxsci/kfn116
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© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Identification of Thioredoxin-2 as a Regulator of the Mitochondrial Permeability Transition

Min He*,{dagger}, Jiyang Cai{ddagger}, Young-Mi Go*, Jennifer M. Johnson*,{dagger}, W. David Martin§, Jason M. Hansen and Dean P. Jones*,1

* Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine {dagger} Graduate Program in Nutrition Health Science; Emory University, Atlanta, Georgia 30322 {ddagger} Vanderbilt Eye Institute, Vanderbilt University Medical Center, Nashville, Tennessee 37232 § Transgenic Mouse Facility Division of Pulmonary, Allergy, Cystic Fibrosis and Sleep, Department of Pediatrics, Emory University, Atlanta, Georgia 30322

1 To whom correspondence should be addressed at Department of Medicine, 205 Whitehead Research Center, Emory University, Atlanta, GA 30322. Fax: (404) 712-2974. E-mail: dpjones{at}emory.edu.

Received March 29, 2008; accepted June 5, 2008


  Abstract

Thioredoxin-2 (Trx2) is a multifunctional, mitochondria-specific protein, which inhibits cell death. The mitochondrial permeability transition (MPT) is a distinct mechanism for cell death activated by oxidants and linked to both necrotic and apoptotic morphologies. We studied mitochondria from Trx2 transgenic mice to determine whether Trx2 protects against oxidant-induced MPT. All experiments were performed in isolated mitochondria. Results showed that Trx2 protected against MPT induced by exogenously added peroxide. Unexpectedly, Trx2 also protected against the MPT induced by Ca2+ in the absence of added peroxide. The results indicate that in addition to protecting against oxidative stress, Trx2 is an endogenous regulator of the MPT.

Key Words: transgenic mice; cell death mechanisms; apoptosis; necrosis; calcium.


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