Regulation of inducible nitric oxide synthase mRNA levels by LPS, INF-gamma, TGF-beta, and IL-10 in murine macrophage cell lines and rat peritoneal macrophages.
Regulation of inducible nitric oxide synthase mRNA levels by LPS, INF-gamma, TGF-beta, and IL-10 in murine macrophage cell lines and rat peritoneal macrophages.
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发表时间：
1994
影响因子：
3.1
通讯作者：
S. Chesrown;J. Monnier;G. Visner;H. Nick
中科院分区：
文献类型：
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作者：
S. Chesrown;J. Monnier;G. Visner;H. Nick
评价LPS、INF-γ、TGF-β和IL-10调节诱导型一氧化氮合酶（iNOS）mRNA表达的分子机制。在小鼠巨噬细胞系中，LPS诱导的iNOS mRNA的增加被放线菌酮或放线菌素D阻断。单独的TGF-β和IL-10对基础表达都没有任何影响，并且每种都仅轻微降低LPS诱导的iNOS mRNA。然而，IL-10增强INF-γ诱导的iNOS mRNA的非常高的水平，而TGF-β抑制INF-γ诱导。人单核细胞表达任何刺激没有可检测的iNOS mRNA，但对人基因组DNA的Southern分析显示了一个特定的人iNOS基因。在人类巨噬细胞中，iNOS基因在进化过程中可能已经变得不稳定。
The molecular mechanisms of LPS, INF-gamma, TGF-beta, and IL-10 regulation of inducible nitric oxide synthase (iNOS) mRNA expression were evaluated. In murine macrophage cell lines, LPS-induced increases in iNOS mRNA were blocked by either cycloheximide or actinomycin D. Neither TGF-beta nor IL-10 alone had any effect on basal expression, and each only slightly reduced LPS induction of iNOS mRNA. However, IL-10 augmented INF-gamma induction of iNOS mRNA to very high levels, while TGF-beta inhibited INF-gamma induction. Human monocytes expressed no detectable iNOS mRNA with any stimuli, though Southern analysis on human genomic DNA revealed a specific human iNOS gene. In human macrophages, the iNOS gene may have become inoperative during evolution.