| Gene name: | PLY |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | BV-2,C6 |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | Senescence of glial cells (BV-2 and C6) was evident by SA-β-gal staining and morphological changes such as enlargement of the cell body and flat shape. Exposure to PLY for 24 h significantly increased the number of SA-β-gal positive cells compared with untreated control cells. PLY induced BV-2 cell cycle arrest in the G0/G1 phase during the 24 h exposure. |
| Regulatory pathway: | MAPK-NF-κB |
| R-AG-Pathway: | Activation |
| Official symbol(s): | MAPK-NFKB1 |
| Pathway experiment: | SA-β-gal activity assay//Western blot//Co-IP |
| Pathway description: | Phosphorylation of ERK1/2, p38 MAPK, and JNK was increased in PLY-treated BV-2 cells .NAC inhibited MAPK activities by pretreatment with for 2 h followed by incubation with PLY for 12 h . Increased expression of PAI-1 in PLY-induced BV-2 cells was significantly decreased by the MAPK inhibitors. In addition, treatment with MAPK inhibitors significantly reduced the number of SA-β-gal positive cells. PLY treatment enhanced the expression of p65 subunit of NF-kB in a time-dependent manner.We also investigated whether the interaction between SIRT-1 and p65 proteins is affected by PLY treatment, given the SIRT-1 interacts with p65 in modulating cell fate in response to various signaling events. The interaction was confirmed by a co-immunoprecipitation assay. SIRT-1 and p65 physically interacted with each other at 4 h or 24 h in PLY-treate BV-2 microglial cells . Altogether, these results suggest that PLY induces cellular senescence via the SIRT-1 and NF-kB interaction in BV-2 cells.All the MAPK pathway inhibitors differentially reduced the expression of p-SIRT-1 and NF-kB enhanced by PLY. |
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