Regulation of manganese superoxide dismutase by lipopolysaccharide, interleukin-1, and tumor necrosis factor. Role in the acute inflammatory response.
Regulation of manganese superoxide dismutase by lipopolysaccharide, interleukin-1, and tumor necrosis factor. Role in the acute inflammatory response.
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DOI：
10.1016/s0021-9258(19)39880-1
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发表时间：
1990-02
期刊：
影响因子：
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通讯作者：
G. Visner;W. Dougall;J. Wilson;I. A. Burr;H. Nick
中科院分区：
文献类型：
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作者：
G. Visner;W. Dougall;J. Wilson;I. A. Burr;H. Nick
我们已经证明了锰超氧化物歧化酶（Mn-SOD） mRNA水平在肺上皮细胞中受到脂多糖（LPS）、白细胞介素-1和肿瘤坏死因子的显著诱导。这些刺激对铜/锌(Cu/Zn)-SOD的mRNA水平没有影响。用LPS对肺成纤维细胞进行相同处理后，Mn-SOD mRNA水平仅发生微小变化，表明这种急性炎症介质具有细胞类型特异性作用。此外，我们已经证明高氧在24小时内对成纤维细胞或上皮细胞中mn或Cu/Zn-SOD mRNA水平没有影响。LPS诱导的Mn-SOD mRNA水平被放线菌素完全抑制。用环己亚胺处理细胞的诱导作用与LPS相同，而环己亚胺和LPS共同处理导致“超级诱导”。这一数据强烈提示Mn-SOD在急性炎症反应中的重要作用。
We have demonstrated a dramatic induction of manganese superoxide dismutase (Mn-SOD) mRNA levels in response to lipopolysaccharide (LPS), interleukin-1, and tumor necrosis factor in pulmonary epithelial cells. These stimuli had no effect on the corresponding mRNA levels for the copper/zinc (Cu/Zn)-SOD. Identical treatments of pulmonary fibroblast cells with LPS showed only minor changes in the Mn-SOD mRNA levels demonstrating a cell type-specific effect for this acute inflammatory mediator. Furthermore, we have shown that hyperoxia has no effect within 24 h on Mn-or Cu/Zn-SOD mRNA levels in either fibroblasts or epithelial cells. The induction of Mn-SOD mRNA levels by LPS is completely inhibited by actinomycin. Treatment of cells with cycloheximide causes an induction equal to that for LPS, whereas co-treatment with cycloheximide and LPS resulted in a "super induction." This data is strongly suggestive of an important role for the Mn-SOD in the acute inflammatory response.