Posttranscriptional regulation of neuronal nitric oxide synthase expression by IFN-γ

被引:15
作者
Chesler, DA
McCutcheon, JA
Reiss, CS
机构
[1] NYU, Dept Biol, New York, NY 10003 USA
[2] NYU, Ctr Neural Sci, New York, NY 10003 USA
[3] NYU, Coll Dent, Dept Biol Sci, New York, NY 10010 USA
[4] NYU, Sch Med, Kaplan Comprehens Canc Ctr, New York, NY 10016 USA
[5] NYU, Sch Med, Dept Microbiol, New York, NY 10016 USA
[6] CUNY Mt Sinai Sch Med, Dept Microbiol, New York, NY 10029 USA
关键词
D O I
10.1089/107999004322813381
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In this report, the mechanism through which interferon-gamma (IFN-gamma) regulates the expression of nitric oxide synthase (NOS-1) in neurons was examined. We have shown previously that IFN-gamma treatment of cells results in a two log inhibition of vesicular stomatitis virus (VSV) production. This inhibition of VSV replication is dependent both in vitro and in vivo on nitric oxide (NO) production by NOS-1. Furthermore, this effect is associated with the increased expression and activity of NOS-1 following IFN-gamma treatment. In vitro, exposure to IFN-gamma prior to infection with VSV is a prerequisite to establish an effective antiviral state, indicating the necessity for a priming event. Neuroblastoma cells (NB41A3) were treated with IFN-gamma or medium and examined for changes in NOS-1 protein and mRNA expression. NOS-1 protein expression was found to be increased after IFN-gamma treatment, and this was associated with increases in both neosynthesis and NOS-1 protein stability. NOS-1 transcription and mRNA levels were unaffected by IFN-gamma treatment. These data demonstrate that IFN-gamma regulates NOS-1 expression through posttranscriptional and posttranslational mechanisms.
引用
收藏
页码:141 / 149
页数:9
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