Abstract:
BACKGROUND:The purpose of this study was to define the redox sensitive cis-acting transcriptional mechanisms that regulate inducible nitric oxide synthase (iNOS) promoter function in the hepatocyte. METHODS:Clonal deletion constructs of the rat hepatocyte iNOS promoter (Genbank X95629; 1845 base pair)-reporter plasmid were transiently transfected into HepG2 cells treated with IL-1 beta and IL-1 beta + hydrogen peroxide. RESULTS:A segment of the promoter upstream from nucleotide -1126 was associated with redox-sensitive augmentation of promoter activity. Site-directed mutagenesis of 2 antioxidant response elements (AREs) was combined with transfection analysis to demonstrate that mutation of the ARE at nt-1347 ablated oxidant stress-mediated activation of the iNOS promoter. CONCLUSIONS:This ARE conveys the redox-sensitive response of the rat iNOS promoter. Hepatocyte iNOS expression is a novel and, as yet, poorly described antioxidant mechanism that is cytokine and redox sensitive and that plays a pleuripotent regulatory role in hepatocellular function in the face of sepsis and shock.
journal_name
Surgeryjournal_title
Surgeryauthors
Punzalan C,Cai C,Schroeder RA,Kuo PCsubject
Has Abstractpub_date
1999-08-01 00:00:00pages
450-5issue
2eissn
0039-6060issn
1532-7361pii
S0039-6060(99)70191-1journal_volume
126pub_type
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