Research Paper Volume 12, Issue 4 pp 3626—3646
NMR-based metabonomic analysis of HUVEC cells during replicative senescence
- 1 College of Chemistry and Chemical Engineering, Key Laboratory for Chemical Biology of Fujian Province, MOE Key Laboratory of Spectrochemical Analysis and Instrumentation, Xiamen University, Xiamen 361005, China
- 2 Department of Medical Chemistry, China Pharmaceutical University, Nanjing 210009, China
- 3 Research and Communication Center of Exercise and Health, Xiamen University of Technology, Xiamen 361024, China
- 4 State Key Laboratory of Cellular Stress Biology, School of Life Science, Xiamen University, Xiamen 361102, China
received: December 17, 2019 ; accepted: January 27, 2020 ; published: February 17, 2020 ;https://doi.org/10.18632/aging.102834
How to Cite
Copyright © 2020 Yi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.