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Soluble Tumor Necrosis Factor Receptor Mediates Cell Proliferation on Lipopolysaccharide-Stimulated Cultured Human Decidual Stromal Cells
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 i...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Molecular Diversity Preservation International (MDPI)
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695263/ https://www.ncbi.nlm.nih.gov/pubmed/19564935 http://dx.doi.org/10.3390/ijms10052010 |
Sumario: | 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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