肌腱源性干细胞/祖细胞衰老：自我更新缺陷和命运改变。
Tendon-derived stem/progenitor cell aging: defective self-renewal and altered fate.
机构信息
Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA.
出版信息
Aging Cell. 2010 Oct;9(5):911-5. doi: 10.1111/j.1474-9726.2010.00598.x.
Abstract
Aging is a major risk factor for tendon injury and impaired tendon healing, but the basis for these relationships remains poorly understood. Here we show that rat tendon- derived stem ⁄ progenitor cells (TSPCs) differ in both self-renewal and differentiation capability with age. The frequency of TSPCs in tendon tissues of aged animals is markedly reduced based on colony formation assays. Proliferation rate is decreased, cell cycle progression is delayed and cell fate patterns are also altered in aged TSPCs. In particular, expression of tendon lineage marker genes is reduced while adipocytic differentiation increased. Cited2, a multi-stimuli responsive transactivator involved in cell growth and senescence, is also downregulated in aged TSPCs while CD44, a matrix assembling and organizing protein implicated in tendon healing, is upregulated, suggesting that these genes participate in the control of TSPC function.
摘要
衰老是肌腱损伤和肌腱愈合受损的一个主要危险因素，但这些关系的基础仍知之甚少。在这里，我们表明，大鼠肌腱衍生的干细胞/祖细胞（TSPCs）在自我更新和分化能力上随年龄而不同。基于集落形成测定，老年动物肌腱组织中的 TSPC 频率明显降低。增殖率降低，细胞周期进程延迟，衰老 TSPC 中的细胞命运模式也发生改变。特别是，肌腱谱系标记基因的表达减少，而脂肪细胞分化增加。Cited2 是一种参与细胞生长和衰老的多刺激反应性转录激活因子，在衰老的 TSPCs 中也下调，而 CD44 是一种与肌腱愈合有关的基质组装和组织蛋白，上调，表明这些基因参与了 TSPC 功能的控制。
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