PMC:4277126 / 8535-10615 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4277126","sourcedb":"PMC","sourceid":"4277126","source_url":"http://www.ncbi.nlm.nih.gov/pmc/4277126","text":"Zebrafish\nCellular senescence can be triggered by a number of factors including aging, DNA damage, oncogene activation, and oxidative stress. Senescence represents a stress response in which cells withdraw from the cell cycle and lose the capability to proliferate in response to growth factors or mitogens. Senescent cells show increased expression of recognized biomarkers of senescence, including staining for β-galactosidase at pH of 6.0 (senescence-associated-β-gal [SA-β-gal]), decreased replicative capacity, and increased expression of p53, p21, p16, and other cyclin-dependent kinase inhibitors, such as p27 and p15.14 p53, a tetrameric transcription factor and tumor suppressor, regulates cell-cycle control, DNA repair, apoptosis, cellular senescence, and cellular stress responses. p53 can promote or inhibit senescence.14 p21 is the first identified downstream target of p53, and it is an essential mediator of p53-dependent cell-cycle arrest. In a recent study, Xia et al15 explored the mechanisms of action of LBPs by phenotypic and SA-β-gal assays, evaluated the survival rates in vivo, and determined expression profiling of genes related to the p53 signaling pathway in a zebrafish model. Zebrafish embryos were continuously exposed to various concentrations of LBPs (1.0 mg/mL, 2.0 mg/mL, 3.0 mg/mL, and 4.0 mg/mL) for 3 days. The results of fluorescent acridine orange and SA-β-gal staining indicated that cell apoptosis and senescence mainly occurred in the head at 24 hours and 72 hours post-fertilization. In addition, resistance to replicative senescence was observed at low doses of LBPs, especially at the 3.0 mg/mL concentration.15 Furthermore, the expression of genes that relate to aging, such as p53, p21, and Bax, was decreased, while Mdm2 (a p53-specific E3 ubiquitin ligase acting as the principal cellular antagonist of p53) and telomerase reverse transcriptase genes were upregulated by LBPs. The results indicate that the beneficial effects of LBPs on cell apoptosis and aging might be mediated by the p53-mediated signaling pathway (Figure 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