Chesrown S E, Monnier J, Visner G, Nick H S
Department of Pediatrics, University of Florida, Gainesville 32610.
Biochem Biophys Res Commun. 1994 Apr 15;200(1):126-34. doi: 10.1006/bbrc.1994.1424.
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.
评估了脂多糖(LPS)、γ干扰素(INF-γ)、转化生长因子-β(TGF-β)和白细胞介素-10(IL-10)对诱导型一氧化氮合酶(iNOS)mRNA表达的调控分子机制。在鼠巨噬细胞系中,LPS诱导的iNOS mRNA增加被放线菌酮或放线菌素D阻断。单独的TGF-β和IL-10对基础表达均无任何影响,且各自仅略微降低LPS对iNOS mRNA的诱导。然而,IL-10将INF-γ对iNOS mRNA的诱导增强至非常高的水平,而TGF-β抑制INF-γ的诱导。尽管对人类基因组DNA进行的Southern分析揭示了一个特定的人类iNOS基因,但人类单核细胞在任何刺激下均未表达可检测到 的iNOS mRNA。在人类巨噬细胞中,iNOS基因可能在进化过程中失去了功能。