| External factors: | Leptin/NAP-2 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | When cultured with UC‐MSCs, both leptin and NAP‐2 increased the percentage of SA β‐gal–positive cells and up‐regulated expression of p53 and p21 in a dose‐dependent manner. Strikingly, concomitant stimulation of UC‐MSCs with leptin and NAP‐2 further increased the frequency of SA β‐gal–positive cells (38.2?±?1.4% versus 24.3?±?0.6% with leptin stimulation alone and 26.0?±?2.0% with NAP‐2 stimulation alone) and increased expression of p53 and p21 compared with stimulation of cells with leptin or NAP‐2 alone, which suggests that these 2 factors act synergistically to affect MSC senescence. |
| Regulatory pathway: | PI3K-Akt |
| R-EF-Pathway: | Activation |
| Official symbol(s): | PIK3CB-AKT |
| Pathway experiment: | SA-β-gal activity assay//Western blot |
| Pathway description: | We indeed demonstrated a substantial, dose‐dependent elevation of phospho‐Akt expression in UC‐MSCs treated with leptin or NAP‐2 . Consistent with this, the senescence induced by leptin and/or NAP‐2 was almost completely reversed after LY294002 treatment, which was demonstrated by a decreased number of SA β‐gal–positive cells and by diminished levels of p53 and p21. |
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