| Gene name: | SPHK1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Adipose stromal cell |
| Experiment: | SA-β-gal activity assay//BrdU assay |
| Description: | A SPHK1 inhibitor, significantly reduced the incorporation of BrdU into cellular DNA compared to control cells,indicative of the lowered proliferative ability.As with high-passage cells,SPHK1-depleted or SKI-treated hAD-SCs underwent accelerated cellular senescence as evidenced by higher SA-β-gal activity. |
| Target gene: | S1P |
| Official symbol(s): | SGPP1 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | SA-β-gal activity assay//BrdU assay |
| Target gene description: | To test this hypothesis, we investigated whether SPHK1 knockdown-induced cellular senescence could be attenuated by inhibition of ceramide synthesis or exogenous supple- NA NA mentation with S1P during cell culture. BrdU incorporation assays showed that the proliferation impeded by shRNA- mediated silencing of SPHK1 could not be recovered by single treatment with S1P or fumonisin B1 (FB1), a ceramide synthesis inhibitor, and even by co-treatment with both , indicating the irreversibility of cellular senescence. In contrast, the elevated activity of SA-β-gal in SPHK1-silenced cells was reduced by simultaneous co-treatment with S1P and FB1, but not by single treatment with either one alone, suggesting that cellular senescence accelerated by SPHK1 depletion may result from increase in ceramide levels with concurrent decrease in S1P levels. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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