Systemic NF-κB-mediated inflammation promotes an aging phenotype in skeletal stem/progenitor cells

被引：0
|
作者：
Josephson, Anne Marie [1 ]
Leclerc, Kevin [1 ]
Remark, Lindsey H. [1 ]
Lopez, Emma Muinos [1 ]
Leucht, Philipp [1 ,2 ]
机构：
[1] NYU Langone Orthoped, NYU Grossman Sch Med, New York, NY 10016 USA
[2] NYU Grossman Sch Med, Dept Cell Biol, New York, NY 10016 USA
来源：
AGING-US | 2021年 / 13卷 / 10期
关键词：
regeneration; skeletal stem cell; aging; inflammation; nuclear factor kappa B; HEMATOPOIETIC STEM; GENE-EXPRESSION; ALPHA; REJUVENATION; ACCUMULATION; ACTIVATION;
D O I：
暂无
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Aging tissues undergo a progressive decline in regenerative potential. This decline in regenerative responsiveness has been attributed to changes in tissue-specific stem cells and their niches. In bone, aged skeletal stem/progenitor cell dysfunction is characterized by decreased frequency and impaired osteogenic differentiation potential. This aging phenotype ultimately results in compromised regenerative responsiveness to injury. The age-associated increase of inflammatory mediators, known as inflamm-aging, has been identified as the main culprit driving skeletal stem cell dysfunction. Here, we utilized a mouse model of parabiosis to decouple aging from inflammation. Using the Nfkb1-/- mouse as a model of inflamm-aging, we demonstrate that a shared systemic circulation between a wild-type and Nfkb1-/- mouse results in an aging phenotype of the wild-type skeletal stem and progenitor cells, shown by CFUfs and osteogenic and adipogenic differentiation assays. Our findings demonstrate that exposure to an inflammatory secretome results in a phenotype similar to the one observed in aging.
引用
收藏
页码：13421 / 13429
页数：9
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