| External factors: | SDB |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | BrdU assay//SA-β-gal activity assay//Western blot |
| Description: | The HFF cell population progressively and irreversibly lost the ability to divide, as assessed by reduced BrdU incorporation in 48 h and reduced cloning efficiency on removal of the SDB.When completely senescent, less than one in 105 cells in the population could form colonies, less than 5% of the cells incorporated BrdU in a 48-h period, and more than 70% expressed SA-βgal. We then proceeded to analyze the senescent-like phenotype generated by SDB at the molecular level.the accumulation of p21WAF precedes that of p16INK4A with the former declining as the latter accumulates [61]. We show that in human fibroblasts treated with SDB the pattern of expression of these two proteins is identical to that found in replicative senescence and that the upregulation of p21WAF coincides with the permanent cell cycle exit of the majority of the cells as assessed by BrdU incorporation and cloning efficiency. |
| Regulatory pathway: | P16-pRb |
| R-EF-Pathway: | -- |
| Official symbol(s): | CDKN2A-RB1 |
| Pathway experiment: | Western blot |
| Pathway description: | FOO3 p16INK4A+/- fibroblasts howed a greater slowing of proliferation and an increased number of flat senescent cells in the population but surprisingly still bypassed SDB-induced stasis when compared to telomerase-expressing HFF dermal fibroblasts. |
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