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通过靶向Sirt1，Nampt表达可降低大鼠骨髓间充质干细胞中与年龄相关的衰老。

Nampt Expression Decreases Age-Related Senescence in Rat Bone Marrow Mesenchymal Stem Cells by Targeting Sirt1.

作者信息

Ma Cao, Pi Chenchen, Yang Yue, Lin Lin, Shi Yingai, Li Yan, Li Yulin, He Xu

机构信息

The Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, China.

Department of Pathology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.

出版信息

PLoS One. 2017 Jan 26;12(1):e0170930. doi: 10.1371/journal.pone.0170930. eCollection 2017.

DOI:10.1371/journal.pone.0170930
PMID:28125705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5268649/
Abstract

Senescence restricts the development of applications involving mesenchymal stem cells (MSCs) in research fields, such as tissue engineering, and stem cell therapeutic strategies. Understanding the mechanisms underlying natural aging processes may contribute to the development of novel approaches to preventing age-related diseases or slowing individual aging processes. Nampt is a rate-limiting NAD biosynthetic enzyme that plays critical roles in energy metabolism, cell senescence and maintaining life spans. However, it remains unknown whether Nampt influences stem cell senescence. In this study, the function of Nampt was investigated using a rat model of natural aging. Our data show that Nampt expression was significantly lower in MSCs obtained from aged rats than in those obtained from young rats during physiological aging. Reducing the level of Nampt in aged MSCs resulted in lower intracellular concentrations of NAD+ and downregulated Sirt1 expression and activity. After the Nampt inhibitor FK866 was added, young MSCs were induced to become aged cells. The enhanced senescence was correlated with NAD+ depletion and Sirt1 activity attenuation. In addition, Nampt overexpression attenuated cell senescence in aged MSCs. Our findings provide a new explanation for the mechanisms underlying stem cell senescence and a novel target for delaying stem cell senescence and preventing and treating age-related diseases.

摘要

衰老限制了间充质干细胞（MSC）在组织工程等研究领域的应用发展以及干细胞治疗策略。了解自然衰老过程的潜在机制可能有助于开发预防与年龄相关疾病或减缓个体衰老过程的新方法。烟酰胺磷酸核糖转移酶（Nampt）是一种限速NAD生物合成酶，在能量代谢、细胞衰老和维持寿命方面发挥着关键作用。然而，Nampt是否影响干细胞衰老仍不清楚。在本研究中，使用自然衰老大鼠模型研究了Nampt的功能。我们的数据表明，在生理衰老过程中，从老年大鼠获得的MSC中Nampt表达明显低于从年轻大鼠获得的MSC。降低老年MSC中Nampt的水平导致细胞内NAD+浓度降低以及Sirt1表达和活性下调。添加Nampt抑制剂FK866后，年轻MSC被诱导成为衰老细胞。衰老增强与NAD+耗竭和Sirt1活性减弱相关。此外，Nampt过表达减轻了老年MSC中的细胞衰老。我们的研究结果为干细胞衰老的潜在机制提供了新的解释，并为延缓干细胞衰老以及预防和治疗与年龄相关疾病提供了新的靶点。

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