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Oxygen tension regulates heme oxygenase-1 gene expression in mammalian cell lines

✍ Scribed by Shigeru Takahashi; Yuji Takahashi; Tatsuya Yoshimi; Takashi Miura

Publisher: John Wiley and Sons
Year: 1998
Tongue: English
Weight: 328 KB
Volume: 16
Category: Article
ISSN: 0263-6484
DOI: 10.1002/(sici)1099-0844(199809)16:3<183::aid-cbf784>3.0.co;2-0

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✦ Synopsis

The gene expression of heme oxygenase-1 (HO-1) was studied in mammalian cell lines exposed to hyperoxia. Northern blot analysis demonstrated that hyperoxic exposure increased the HO-1 mRNA levels in various types of cells, including human hepatoma (HepG2) cells. This increase was time-and dose-dependent, and reversible. The HO-1 mRNA levels in HepG2 cells were increased to 2 . 3-and 4 . 2-fold of the control by hyperoxic exposure of 6 and 23 h, respectively. Cycloheximide and actinomycin D inhibited the increases in the HO-1 mRNA level produced by hyperoxia, indicating that response to hyperoxia is dependent on de novo protein synthesis and mRNA transcription. Antioxidants, desferrioxamine (DES) and o-phenanthroline (OP) partially inhibited the HO-1 mRNA elevation by hyperoxia. In addition to hyperoxia, sodium arsenite (NaAsO 2 ), cadmium chloride (CdCl 2 ) and hydrogen peroxide (H 2 O 2 ), which are reactive oxygen intermediates (ROI) generators, increased the HO-1 mRNA level by 11-, 22-and 2 . 5-fold, respectively. OP, an antioxidant and a bivalent metal chelator, blocked the HO-1 mRNA elevation induced either by hyperoxia or by the three ROI generators. In contrast to OP, N-acetylcysteine (NAC), an antioxidant and membrane-permeable reducing reagent, enhanced the HO-1 mRNA elevation induced by hyperoxia, although NAC inhibited the mRNA elevation induced by NaAsO 2 , CdCl 2 and H 2 O 2 . These results indicate that oxygen tension regulates HO-1 gene expression and suggest that hyperoxia-speci®c and redox-sensitive regulators may be involved in hyperoxia-mediated HO-1 gene expression.

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