NDLI: Thioredoxin restores nitric oxide-induced inhibition of protein kinase C activity in lung endothelial cells

Content Provider	Springer Nature Link
Author	Kahlos, Katriina Zhang, Jianliang Block, Edward R. Patel, Jawaharlal M.
Copyright Year	2003
Abstract	We previously reported that exposure to exogenous nitric oxide (NO) causes diminished expression of thioredoxin/thioredoxin reductase, a critical component of the redox system that regulates the functions of redox-sensitive enzymes, receptors, and transcription factors. Here we examined the role of thioredoxin in NO-induced inhibition of protein kinase C (PKC) isoform(s) and potential interaction of PKC and thioredoxin in pulmonary artery endothelial cells (PAEC) in culture. Exposure to NO gas (8 ppm) significantly diminished the catalytic activity of the representative isoforms of the conventional, novel, and atypical PKCs α,ε, and ζ, respectively, in PAEC. Further examination of NO's effect on PKC-ζ revealed that NO-induced inhibition of the catalytic activity of PKC-ζ was time-dependent and regulated by a posttranscriptional mechanism. NO-induced loss of the catalytic activity of PKC-ζ was restored by incubation with the disulfide reducing agent dithiothreitol (DTT) as well as by purified thioredoxin or thioredoxin reductase. Confocal imaging studies revealed co-localization of PKC and thioredoxin in PAEC. These results indicate that: (1) NO-induced inhibition of PKC isoforms is associated with S-nitrosylation-mediated disulfide formation of active site thiols in PKC-ζ as the disulfide reducing agent DTT and/or the thioredoxin enzyme system restore PKC-ζ catalytic activity and (2) NO causes oxidation of endogenous thioredoxin as exogenous reduced thioredoxin or thioredoxin reductase are required to reduce thioredoxin and to restore the catalytic activity of PKC-ζ in PAEC.
Starting Page	47
Ending Page	54
Page Count	8
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	254
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2003-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cardiology Medical Biochemistry Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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