External factors
| External factors: |
reconstituted HDL |
| 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). |
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Regulatory relationship
| Regulatory pathway:
|
mTORC2-Akt |
| Official symbol(s): |
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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. |
Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.