| External factors: | Amyloid beta oligomer |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Other |
| Phenotype: | Aging |
| Experiment: | Cell morphological analysis//SA-β-gal activity assay |
| Description: | S1A and S1B, HBMECs exposed to Aβ1–42 oligomers showed increased senescence-associated β-galactosidase staining (> 60% compared to ~23% in controls), confirming a senescent phenotype.Using optical microscopy, we observed that the morphology of β-galactosidase positive Aβ1–42 oligomer treated HBMECs displayed a mixed population of normal appearing cells as well as enlarged cells with a flatter and spread-out nucleus, the latter being a characteristic feature of senescent cells. |
| Target gene: | VEGFR-1//RAC1 |
| R-EF-Target gene: | Upregulation//Downregulation |
| Official symbol(s): | FLT1//RAC1 |
| Target gene experiment: | Western blot |
| Target gene description: | Furthermore, we showed that VEGFR-1 was highly upregulated in HBMECs following treatment with Aβ1 42 oligomers and knockdown of VEGFR-1 significantly reduced Aβ1 42 oligomerinduced senescence in the HBMECs, suggesting a key role of VEGRF-1 expression and signaling in this paradigm.Quantification of the western blot showed a significant reduction in Rac 1 protein levels in the senescent HBMECs (~40 50% reduction compared to untreated controls. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: