Soluble tumor necrosis factor receptor mediates cell proliferation on lipopolysaccharide-stimulated cultured human decidual stromal cells.

Soluble tumor necrosis factor receptor mediates cell proliferation on lipopolysaccharide-stimulated cultured human decidual stromal cells.
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DOI:
10.3390/ijms10052010
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发表时间:
2009-05-04
影响因子:
5.6
通讯作者:
Li X
Li X
中科院分区:
生物学2区
文献类型:
--
作者:
Yu XW;Zhang XW;Li X

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肿瘤坏死因子-α(TNF-α)细胞因子受体系统调节许多细胞类型的凋亡,因此我们研究了sTNFR 1在细菌脂多糖(LPS)诱导的培养人蜕膜基质细胞死亡中的作用,假设sTNFR 1可能在此作用中发挥核心作用。在这项工作中,我们的特点是在体外蜕膜基质细胞的活力与LPS处理和LPS和sTNFR 1的共同处理。我们发现LPS处理以剂量依赖性方式诱导蜕膜基质细胞死亡,并且sTNFR 1阻断LPS处理的效果。与0.01、0.05、0.2和0.5 μg/mL的LPS和sTNFR 1相比,在与10 μg/mL的LPS和0.1 μg/mL的sTNFR 1共孵育的细胞中有显著的增殖(p < 0.01)。本研究表明,在体外LPS导致蜕膜基质细胞死亡,但sTNFR 1下调细胞死亡,由于LPS在相同的条件下。综上所述,这些结果表明sTNFR 1可以参与针对内毒素的保护机制。
The tumor necrosis factor-alpha (TNF-α) cytokine receptor system modulates apoptosis in many cell types, so we have investigated the role of sTNFR1 in bacterial lipopolysaccharide (LPS)-induced cell death in cultured human decidual stromal cells, hypothesizing that sTNFR1 might play a central role in this action. In this work we characterized in vitro decidual stromal cell viability with LPS treatment and LPS and sTNFR1 co-treatment. We found that LPS treatment induced decidual stromal cell death in a dose-dependent manner and that sTNFR1 blocked the effect of the LPS treatment. There was a significant proliferation among cells co-incubated with LPS at 10 μg/mL and sTNFR1 at 0.1 μg/mL compared with LPS and sTNFR1 at 0.01, 0.05, 0.2 and 0.5 μg/mL (p < 0.01). This study demonstrated that LPS led to decidual stromal cell death in vitro but sTNFR1 down-regulates the cell death due to LPS under the same conditions. Taken together, these results suggested that sTNFR1 could participate in a protective mechanism against endotoxin.
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