| External factors: | IL-6/sIL-6R |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Cell morphological analysis |
| Description: | We assessed two biomarkers characteristic of most senescent cells, morphological changes and SA-β-Gal activity.13 TIG3 cells treated with IL-6/sIL-6R for 8 d showed both an enlarged and flattened morphology and increased SA-β-Gal activity, indicating that IL-6/sIL-6R stimulation can cause premature senescence in young TIG3 fibroblasts in the culture conditions used here. |
| Target gene: | P15INK4B (CDKN2B)//STAT3//IGFBP5 |
| R-EF-Target gene: | Upregulation//--//-- |
| Official symbol(s): | P15INK4B (CDKN2B)//STAT3//IGFBP5 |
| Target gene experiment: | Western blot//qRT-PCR |
| Target gene description: | This IL-6-induced premature senescence was accompanied by increased levels of the cyclin-dependent kinase inhibitor p15INK4b (CDKN2B).The mRNA levels for all four factors increased on days 4 and 5 after IL-6/sIL-6R stimulation, and rapidly decreased thereafter. The levels were markedly reduced in TIG3 cells expressing HA-STAT3F.Consistent with this, TIG3/IGFBP5KD cells showed a much poorercellular senescence response to IL-6/sIL-6R compared with control TIG3 cells , indicating that IGFBP5 induction is important for the IL-6/sIL-6R-induced premature senescence. |
| Regulatory pathway: | p53 |
| R-EF-Pathway: | -- |
| Official symbol(s): | TP53 |
| Pathway experiment: | Knockdown//SA-β-gal activity assay |
| Pathway description: | Knocking down p53 markedly decreased the SA-β-Gal activity in TIG3 cells stimulated with IL-6/sIL-6R and caused continuous proliferation (data not shown). This indicates that p53 is essential for the IL6/sIL-6R-induced premature senescence. |
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