期刊
BRAIN RESEARCH BULLETIN
卷 52, 期 3, 页码 155-161出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0361-9230(00)00262-8
关键词
nitric oxide; NF-kappa B; I kappa B; Rel proteins; HIV-1; glial cells
Nitric oxide (NO) has been reported to regulate NF-kappa B, one of the best-characterized transcription factors playing important roles in many cellular responses to a large variety of stimuli. NO has been suggested to induce or inhibit the activation of NF-kappa B, its effect depending, among others, on the cell type considered. In this review, the inhibitory effect of NO on NF-kappa B (and subsequent suppression of NF-kappa B-dependent gene expression) in glial cells is reported. In particular, exogenous end endogenous NO has been observed to keep NF-kappa B suppressed, thus preventing the expression of NF-kappa B-induced genes, such as inducible NO synthase itself or HIV-1 long terminal repeat. Furthermore, the possible molecular mechanisms of NO-mediated NF-kappa B inhibition are discussed. More specifically, NO has been reported to suppress NF-kappa B activation inducing and stabilizing the NF-kappa B inhibitor, I kappa B-alpha. On the other hand, NO may inhibit NF-kappa B DNA binding through S-nitrosylation of cysteine residue (i.e., Cys62) of the p50 subunit. As a whole, a novel concept that the balance of intracellular NO levels may control the induction of NF-kappa B in glial cells has been hypothesized. (C) 2000 Elsevier Science Inc.
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