期刊
AGING CELL
卷 11, 期 2, 页码 345-349出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1474-9726.2012.00795.x
关键词
aging; DNA damage; 53BP1; GFP; fluorescence; cell signalling
资金
- BBSRC [BB/C008200/1 (CISBAN)]
- MRC/Unilever Biomarker grant [G0601333]
- BBSRC/Procter Gamble CASE
- BBSRC [BB/F010966/1, BB/I020748/1] Funding Source: UKRI
- MRC [G0601333, G0900686] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/I020748/1, BB/F010966/1] Funding Source: researchfish
- Medical Research Council [G0601333, G0900686] Funding Source: researchfish
Senescent cells produce and secrete various bioactive molecules including interleukins, growth factors, matrix-degrading enzymes and reactive oxygen species (ROS). Thus, it has been proposed that senescent cells can damage their local environment, and a stimulatory effect on tumour cell growth and invasiveness has been documented. However, it was unknown what effect, if any, senescent cells have on their normal, proliferation-competent counterparts. We show here that senescent cells induce a DNA damage response, characteristic for senescence, in neighbouring cells via gap junction-mediated cellcell contact and processes involving ROS. Continuous exposure to senescent cells induced cell senescence in intact bystander fibroblasts. Hepatocytes bearing senescence markers clustered together in mice livers. Thus, senescent cells can induce a bystander effect, spreading senescence towards their neighbours in vitro and, possibly, in vivo.
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