| External factors: | ZnPyr |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay |
| Description: | ZnPyr at the concentration of 125 nM markedly increased the expression of the aforementioned marker with the first significant changes occurring as early as at 6 h of treatment and with the maximum expression observed at 24 h of treatment. |
| Target gene: | P53//P38//NAC |
| R-EF-Target gene: | --//--//-- |
| Official symbol(s): | P53//P38//NAC |
| Target gene experiment: | SA-β-gal activity assay//Knockdown |
| Target gene description: | The results suggested that both oxidative stress and p53 play an important role in ZnPyr induced apoptosis. Similarly, 125 nM ZnPyr-stimulated premature senescence was targeted using the above mentioned manipulations. The rate of premature senescence in thus treated cells was slightly reduced in the presence of NAC. Conversely, both p38 and p53 knockdown significantly decreased the number of cells with premature senescence phenotype and this decrease was even more marked when both targets were inhibited simultaneously. |
| Regulatory pathway: | mTOR |
| R-EF-Pathway: | -- |
| Official symbol(s): | MTOR |
| Pathway experiment: | SA-β-gal activity assay//Western blot |
| Pathway description: | Finally, mTOR pathway which is known to influence proliferation-senescence axis in cells was investigated in ZnPyr-treated fibroblasts. The results indicated its inhibition upon 500 nM ZnPyr treatment while 125 nM ZnPyr exposure had an opposite effect .mTOR-specific inhibitor had a significant effect on ZnPyrinduced premature senescence too. |
Annotation: