| External factors: | PGE2 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//MTT assay//BrdU assay |
| Description: | Treatment with PGE2 increases SA-β-gal activity and decreases cell proliferation in a dose and time-dependent manner. Since PGE2 stimulates cell proliferation in vascular smooth muscle cells (Yau and Zahradka 2 3) and esophageal cancer cells ,we treated cells with submicromolar concentrations of PGE2and measured cell proliferation by cell counting. No significant reduction or increase in cell proliferation was observed in cells treated with up to 1 lM PGE2. A decrease in cell proliferation by PGE2 treatment was further confirmed by the reduction of intracellular BrdU incorporation in PGE2-treated cells. |
| Target gene: | IGFBP5 |
| R-EF-Target gene: | Upregulation |
| Official symbol(s): | IGFBP5 |
| Target gene experiment: | RT-PCR//Western blot//Luciferase reporter assay//SA-β-gal activity assay |
| Target gene description: | The expression levels of IGFBP5 mRNA were measured in cells treated with PGE2 or forskolin. Both PGE2 and forskolin increase IGFBP5 mRNA levels. As expected, IGFBP5 protein levels are also enhanced by forskolin. The PGE2-induced increase of IGFBP5 protein expression could be decreased by pretreatment with EP1 and EP4 receptor antagonists. To test whether the increased levels of IGFBP5 mRNA and protein by PGE2 and forskolin treatment is mediated by promoter activation, plasmids containing luciferase controlled by the IGFBP5 promoter were transfected into AD293 cells and luciferase activity was measured after PGE2 treatment. After 48 h of PGE2 treatment, luciferase activity increases by fourfold. PGE2-induced increases in SA-β-gal activity and p53 protein level are repressed by IGFBP5 knockdown. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: