Induction of thioredoxin and mitochondrial survival proteins mediates preconditioning-induced cardioprotection and neuroprotection

Juang-Ching Chiue, Tsugunobu Andoh, P. Boon Chock

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

Delayed cardio- and neuroprotection are observed following a pre-conditioning procedure evoked by a brief and nontoxic oxidative stress due to deprivation of oxygen, glucose, serum, trophic factors, and/or antioxidative enzymes. Preconditioning protection can be observed in vivo and is under clinical trials for preservation of cell viability following organ transplants of liver. Previous studies indicated that ischemic preconditioning increases the expression of heat-shock proteins (HSPs) and nitric oxide synthase (NOS). Our pilot studies indicate that the treatment of neuronal NOS inhibitor (7-nitroindazole) and 6Br-cGMP blocks and mimics, respectively, preconditioning protection in human neuroblastoma SH-SY5Y cells. This minireview focuses on nitric oxide-mediated cellular adaptation and the related cGMP/PKG signaling pathway in a compensatory mechanism underlying preconditioning-induced hormesis. Both preconditioning and 6Br-cGMP increase the induction of human thioredoxin (Trx) mRNA and protein for cytoprotection, which is largely prevented by transfection of cells with Trx antisense but not sense oligonucleotides. Cytosolic Trx1 and mitochondrial Trx2 suppress free radical formation, lipid peroxidation, oxidative stress, and mitochondria-dependent apoptosis; knock out/ down of either Trx1 or Trx2 is detrimental to cell survival. Other recent findings indicate that a transgenic increase of Trx in mice increases tolerance against oxidative nigral injury caused by 1-hiethyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP). Trx1 can be translocated into nucleus and phosphoactivated CKEB for a delayed induction of mitochondrial anti-apoptotic Bcl-2 and antioxidative MnSOD that is known to increase vitality and survival of cells in the brain and the heart. In conclusion, preconditioning adaptation or a brief oxidative stress induces a delayed nitric oxide-mediated compensatory mechanism for cell survival and vitality in the central nervous system and the cardiovascular system. Preconditioning-induced adaptive tolerance may be signaling through a cGMP-dependent induction of cytosolic redox protein Trx1 and subsequently mitochondrial proteins such as Bcl-2, MnSOD, and perhaps Trx2 or HSP70.

Original languageEnglish
Pages (from-to)403-418
Number of pages16
JournalAnnals of the New York Academy of Sciences
Volume1042
DOIs
Publication statusPublished - 2005

Fingerprint

Thioredoxins
Mitochondrial Proteins
Oxidative stress
Cell Survival
Cells
Oxidative Stress
Survival
Nitric Oxide
Proteins
Hormesis
Cardiovascular system
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Ischemic Preconditioning
Nitric Oxide Synthase Type I
Transplants
Mitochondria
Cytoprotection
Neurology
Substantia Nigra
Cardiovascular System

Keywords

  • Adaptation
  • ATP-sensitive potassium channel/K(ATP)
  • Bcl-2
  • Cyclic GMP
  • MnSOD
  • Nitric oxide (NO)
  • Nitric oxide synthase (NOS)
  • Thioredoxin

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Induction of thioredoxin and mitochondrial survival proteins mediates preconditioning-induced cardioprotection and neuroprotection. / Chiue, Juang-Ching; Andoh, Tsugunobu; Chock, P. Boon.

In: Annals of the New York Academy of Sciences, Vol. 1042, 2005, p. 403-418.

Research output: Contribution to journalArticle

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