| External factors: | reconstituted HDL |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Other |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay |
| Description: | Treatment with 50, 100, or 150 μg/mL rHDL reduced the number of acidic β-gal+ CACs and improved the △Ψ of CACs (data not shown). |
| Regulatory pathway: | mTORC2-Akt |
| R-EF-Pathway: | Activation |
| Official symbol(s): | AKT1 |
| Pathway experiment: | IP//Western blot//SA-β-gal activity assay |
| Pathway description: | Akt-Ser473 phosphorylation increased after 10 minutes and peaked after ≈4 hours , whereas the total Akt level remained unchanged. mTOR formed a complex with rictor in rHDL-treated CACs, whereas rapamycin inhibited the coprecipitation of both proteins.Control siRNA had no effect. The siRNA-treated CACs next were cocultured with rHDL for 4 hours. The siRNA-mediated suppression of rictor gene expression significantly decreased the rHDL-induced Akt phosphorylation compared with control siRNA transfection, whereas siRNA-mediated raptor suppression had no effect. Suppression of rictor gene expression also abolished the inhibitory effect of rHDL on CAC senescence. |
Annotation: