| External factors: | Cigarette smoke |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Other |
| Phenotype: | Chronic obstructive pulmonary disease |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Immunofluorescence |
| Description: | A time-dependent increase in cellular senescence was observed in HFL1 and mouse primary lung fibroblasts, which was characterized by increased SA-β-gal activity. Using a fluorogenic senescence marker (C12FDG), we quantified the degree of cellular senescence by flow cytometry, which showed an increase in cellular senescence by CSE.Our results show increased p16 and p21 levels, as well as DNA damage, measured in terms of g-H2AX foci formation [catalog number Ab2893 (Abcam) and catalog number 05-636 (EMD Millipore, Billerica, MA, USA)] in CSE-treated HFL1 cells, which confirmed the establishment of cellular senescence in an in vitro model. |
| Target gene: | PARKIN |
| R-EF-Target gene: | -- |
| Official symbol(s): | PARKIN |
| Target gene experiment: | Immunofluorescence |
| Target gene description: | However, Parkin (catalog number 2132S; Cell Signaling Technology) mitochondrial translocation was highly impaired in HFL1 cells by CSE . |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: