| External factors: | 5‐FU |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//BrdU assay//Cell morphological analysis//DAPI staining |
| Description: | Short‐term exposure to 5FU caused profound alterations in EA.hy926 cells, overall indicating senescence. Positivity for SA β‐gal and p16INK4a significantly increased , whilst proliferation was inhibited . Morphologically, 5FU‐treated cells displayed an enlarged, flattened cytoplasm with a ‘fried egg’ appearance . These phenotypic changes were associated with the up‐regulation of the genes encoding VCAM‐1 and – although not to a significant extent – ICAM‐1, consistent with earlier evidence of a dysfunctional activation of endothelial cells undergoing senescence . |
| Target gene: | P38//JNK//ENOS//SIRT1 |
| R-EF-Target gene: | --//--//Downregulation//Downregulation |
| Official symbol(s): | P38//MAPK8//ENOS//SIRT1 |
| Target gene experiment: | SA-β-gal activity assay//Western blot//Densitometry analysis |
| Target gene description: | Induction of senescence by 5FU, as assessed by staining for SA β‐gal, was significantly reduced by inhibiting p38 and JNK, suggesting the involvement of these kinases. Compared with control, 5FU decreased the expression of both eNOS and SIRT1. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: