Downregulation of FOXP1 correlates with tendon stem/progenitor cells aging.
[No authors listed]
摘要
Aging is known as a major risk factor for tendon disorders whereas the molecular mechanisms of age-related tendon disorders still remains unclear. Since tendon-derived stem/progenitor cells (TSPCs) play a vital role in tendon maintenance and healing, in this study we aimed to investigate the role of Forkhead box P1 (FOXP1) in aged TSPCs, we found that FOXP1 mRNA and protein levels were markedly decreased in the aged TSPCs. Moreover, overexpression of FOXP1 attenuates TSPCs aging, as confirmed by decreased of senescence-associated β-gal staining, as well as the senescence marker, p16INK4A. Conversely, FOXP1 depletion by siRNA promoted senescence in young TSPCs. Meanwhile, FOXP1 overexpression also restores the age-associated reduction of self-renewal, migration and differentiation of TSPCs. In addition, FOXP1 overexpression rescued decreased levels of E2F1, pRb and cyclin D1 in aged TSPCs, which suggested that FOXP1 regulates TSPCs aging through cellular senescence. These results indicate that FOXP1 plays a crucial role in TSPCs aging.
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基因功能
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原始数据
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文献解读
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