复制性衰老过程中HUVEC细胞的基于NMR的代谢组学分析。,Aging-US

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复制性衰老过程中HUVEC细胞的基于NMR的代谢组学分析。
Aging-US ( IF 3.9 ) Pub Date : 2020-02-17 , DOI: 10.18632/aging.102834
Shenghui Yi _{1,

2} , Kejiang Lin ₂ , Ting Jiang ₁ , Wei Shao ₁ , Caihua Huang ₃ , Bin Jiang ₄ , Qinxi Li ₄ , Donghai Lin ₁

Affiliation

细胞衰老是对刺激作出反应的生理过程，其中细胞响应与代谢紊乱相关的不良后果而进入不可逆的生长停滞状态。尚不清楚细胞衰老进展的分子机制。在这里，我们建立了人类脐静脉内皮细胞（HUVEC）从第3代（P3）到第18代（P18）的复制衰老模型，并进行了生化表征和基于NMR的代谢组学分析。随着细胞在体外相继传代，细胞衰老程度提高，并且细胞代谢谱逐渐改变。与P3细胞相比，分别在P6，P10，P14和P18细胞中主要共有8、16、21和19种重要的代谢物发生了主要变化。这些代谢物主要参与14个显着改变的代谢途径。此外，我们观察到牛磺酸可延缓衰老引起的氧化损伤。在能量不足的情况下，HUVEC会代谢中性氨基酸以补充能量，从而在细胞衰老的早期增加谷氨酰胺，天冬氨酸和天冬酰胺，但在后期则降低。我们的结果表明，细胞复制衰老与氧化应激的增强，能量代谢受损和蛋白质合成受阻密切相关。这项工作可以提供对细胞衰老进展的机械理解。HUVEC代谢中性氨基酸以补充能量，因此在细胞衰老的早期增加了谷氨酰胺，天冬氨酸和天冬酰胺，但在后期则降低了谷氨酸。我们的结果表明，细胞复制衰老与氧化应激的增强，能量代谢受损和蛋白质合成受阻密切相关。这项工作可以提供对细胞衰老进展的机械理解。HUVEC代谢中性氨基酸以补充能量，因此在细胞衰老的早期增加了谷氨酰胺，天冬氨酸和天冬酰胺，但在后期则降低了谷氨酸。我们的结果表明，细胞复制衰老与氧化应激的增强，能量代谢受损和蛋白质合成受阻密切相关。这项工作可以提供对细胞衰老进展的机械理解。

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NMR-based metabonomic analysis of HUVEC cells during replicative senescence.

Cellular senescence is a physiological process reacting to stimuli, in which cells enter a state of irreversible growth arrest in response to adverse consequences associated with metabolic disorders. Molecular mechanisms underlying the progression of cellular senescence remain unclear. Here, we established a replicative senescence model of human umbilical vein endothelial cells (HUVEC) from passage 3 (P3) to 18 (P18), and performed biochemical characterizations and NMR-based metabolomic analyses. The cellular senescence degree advanced as the cells were sequentially passaged in vitro, and cellular metabolic profiles were gradually altered. Totally, 8, 16, 21 and 19 significant metabolites were primarily changed in the P6, P10, P14 and P18 cells compared with the P3 cells, respectively. These metabolites were mainly involved in 14 significantly altered metabolic pathways. Furthermore, we observed taurine retarded oxidative damage resulting from senescence. In the case of energy deficiency, HUVECs metabolized neutral amino acids to replenish energy, thus increased glutamine, aspartate and asparagine at the early stages of cellular senescence but decreased them at the later stages. Our results indicate that cellular replicative senescence is closely associated with promoted oxidative stress, impaired energy metabolism and blocked protein synthesis. This work may provide mechanistic understanding of the progression of cellular senescence.

更新日期：2020-02-17

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