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首页> 外文期刊>American Journal of Physiology >Synergistic regulation of NOS II expression by IL-1 beta and TNF-alpha in cultured rat colonic smooth muscle cells.
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Synergistic regulation of NOS II expression by IL-1 beta and TNF-alpha in cultured rat colonic smooth muscle cells.

机译：IL-1β和TNF-α在培养的大鼠结肠平滑肌细胞中对NOS II表达的协同调节。

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摘要

Interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and lipopolysaccharide (LPS) were examined for their ability to regulate the activity and protein levels of inducible nitric oxide synthase (NOS II) in cultured rat colonic smooth muscle cells. Treatment with these agents resulted in a time-dependent increase in NOS II activity. After 48 h, NOS II activity, measured as L-[3H]citrulline production, was increased 24.3 +/- 6.9 pmol.min-1.mg protein-1 by 1 nM IL-1 beta and 3.2 +/- 1.1 pmol.min-1.mg protein-1 by 1 nM TNF-alpha, and increased synergistically by a combination of the two (51.8 +/- 7.3 pmol.min-1.mg protein-1). Measurement of NOS II activity as nitrite production yielded similar results: IL-1 beta, 27.2 +/- 1.2; TNF-alpha, 1.6 +/- 0.1; and IL-1 beta + TNF-alpha, 46.8 +/- 3.2 pmol.min-1.mg protein-1 above basal. LPS (10 micrograms/ml) had a small but significant effect at 48 h that was only additive with that of IL-1 beta. The increase in NOS II activity induced by IL-1 beta and TNF-alpha was inhibited 73-86% by transforming growth factor-beta 1 (TFG-beta 1). The NOS isoform induced by IL-1 beta and TNF-alpha was identified as NOS II by Western immunoblot analysis and confirmed by its 66-97% inhibition by 100 microM S-methylisothiourea, a selective NOS II inhibitor, and its Ca(2+)-independent activity. We conclude that the cytokines IL-1 beta and TNF-alpha act independently and synergistically to stimulate NOS II expression and enzymatic activity in rat colonic smooth muscle through a mechanism sensitive to inhibition by TGF-beta 1.
机译：检查了白介素-1 beta（IL-1 beta），肿瘤坏死因子-α（TNF-alpha）和脂多糖（LPS）调节培养的诱导型一氧化氮合酶（NOS II）的活性和蛋白质水平的能力。大鼠结肠平滑肌细胞。用这些药物治疗导致NOS II活性随时间增加。 48小时后，以1 L- [3H]瓜氨酸产量衡量的NOS II活性通过1 nM IL-1 beta和3.2 +/- 1.1 pmol增加了24.3 +/- 6.9 pmol.min-1.mg蛋白-1。 min-1.mg蛋白-1增加1 nM TNF-alpha，并通过两者的组合协同增加（51.8 +/- 7.3 pmol.min-1.mg protein-1）。测量亚硝酸盐产生时NOS II活性产生相似的结果：IL-1 beta，27.2 +/- 1.2; TNF-α，1.6 +/- 0.1; IL-1 beta + TNF-alpha，高于基础水平46.8 +/- 3.2 pmol.min-1.mg蛋白-1。 LPS（10微克/毫升）在48 h时产生的作用很小但很明显，仅与IL-1 beta产生了作用。 IL-1β和TNF-α诱导的NOS II活性增加被转化生长因子-β1（TFG-β1）抑制了73-86％。 IL-1β和TNF-α诱导的NOS亚型通过Western免疫印迹分析鉴定为NOS II，并通过100 microM S-甲基异硫脲，一种选择性NOS II抑制剂及其Ca（2+ ）独立活动。我们得出的结论是，细胞因子IL-1β和TNF-α通过对TGF-β1抑制敏感的机制独立和协同地刺激大鼠结肠平滑肌中NOS II表达和酶活性。

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