External factors: | Aβ1-42 oligomers |
Aging type: | Accelerate |
Aging characteristic: |
Category: | Chemical compounds |
Phenotype: | Alzheimer's disease |
Experiment: | SA-β-gal activity assay// Western blot |
Description: | HBMECs exposed to Aβ1-42 oligomers appeared flattened and enlarged and showed increased senescence-associated β-galactosidase staining, exhibiting hallmark features of a senescent phenotype.Western blot analysis showed significantly increased p21 protein levels in the Aβ1-42 oligomer-treated HBMECs compared with control group. |
Regulatory pathway: | VEGFR//p21-p53 |
R-EF-Pathway: | Upregulation//Upregulation |
Official symbol(s): | KDR//CDKN1A-TP53 |
Pathway experiment: | Western blot//qRT-PCR |
Pathway description: | Upon Aβ1-42 oligomer treatment, we observed a significant increase in VEGFR-1 protein levels, whereas protein levels of VEGFR-2 were not significantly altered.Western blot analysis showed significantly increased VEGFR-1 protein levels only in the Aβ1-42 oligomer-treated HBMECs but not in either Aβ1-42 monomers or Aβ1-42 fibrils-treated HBMECs .Western blotting analysis from chimeric receptor EGLT-transfected lysates confirmed the increased expression of the VEGFR-1 protein and increased p21 proteins levels and decreased expression of VEGFR-2 levels. qRT-PCR analysis showed increased mRNA levels of VEGFR-1, p21,and p53. There was a decrease in the p53 isoform Δ133p53 mRNA levels and no significant changes in p53b or VEGFR-2 mRNA levels.Western blot analysis showed increased levels of VEGFR-1 and p21 protein expression following Aβ1-42 oligomer treatment compared with control groups as previously shown. |
Annotation: