期刊
DEVELOPMENTAL CELL
卷 31, 期 6, 页码 722-733出版社
CELL PRESS
DOI: 10.1016/j.devcel.2014.11.012
关键词
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资金
- American Italian Cancer Foundation
- Japan Science and Technology Agency
- U.S. NIH [AG017242, AG009909, AG041122, CA166347]
- European Council Advanced Grant [GA233424]
Cellular senescence suppresses cancer by halting the growth of premalignant cells, yet the accumulation of senescent cells is thought to drive age-related pathology through a senescence-associated secretory phenotype (SASP), the function of which is unclear. To understand the physiological role(s) of the complex senescent phenotype, we generated a mouse model in which senescent cells can be visualized and eliminated in living animals. We show that senescent fibroblasts and endothelial cells appear very early in response to a cutaneous wound, where they accelerate wound closure by inducing myofibroblast differentiation through the secretion of platelet-derived growth factor AA (PDGF-AA). In two mouse models, topical treatment of senescence-free wounds with recombinant PDGF-AA rescued the delayed wound closure and lack of myofibroblast differentiation. These findings define a beneficial role for the SASP in tissue repair and help to explain why the SASP evolved.
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