| Gene name: | PLK1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HDF,HUVEC |
| Experiment: | Western blot//SA-β-gal activity assay//Cell counting//BrdU assay//Cell morphological analysis |
| Description: | Replicative senescence in cells was confirmed by increases in SA-β-gal staining and the levels of p53, p21, and p16 proteins as well as enlarged, flattened cell morphology . The expression levels of PLK1 mRNA and protein decreased in old cells compared with young cells. PLK1 immunoreactivity was stronger in young cells than in old cells and PLK1 was localized in the nucleus or chromosomes of young cells under mitosis . Furthermore, the level of PLK1 protein also decreased during adriamycin-induced premature cellular senescence.Following transduction of old cells with recombinant PLK1 adenovirus, upregulation of PLK1 protein levels was confirmed by Western blot analysis. PLK1 overexpression in old cells increased cell proliferation , BrdU incorporation, and PDs . PLK1 upregulation decreased SA-β-gal staining in a dose-dependent manner. |
| Regulatory pathway: | P53 |
| R-AG-Pathway: | -- |
| Official symbol(s): | TP53 |
| Pathway experiment: | Knockdown//Western blot//Cell counting//SA-β-gal activity assay |
| Pathway description: | Downregulation of p53, p21, and PLK1 was confirmed by Western blotting. However, we could hardly detect the p16 protein in our experimental condition because young cells were known to express very low level of p16 protein in normal condition. Instead, we confirmed the knockdown of p16 by transfecting old cells with the p16 shRNA vector since old cells show an increase in the p16 level. Although p16 shRNA–treated cells showed senescence phenotypes induced by PLK1 knockdown, such as decreased cell proliferation and increased SA-β-gal staining, p53 shRNA–treated cells did not. |
Annotation:
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