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Int. J. Mol. Sci. 2018, 19(7), 1997; https://doi.org/10.3390/ijms19071997

Senescence Induces Dysfunctions in Endothelial Progenitor Cells and Osteoblasts by Interfering Translational Machinery and Bioenergetic Homeostasis

1
Department of Orthopaedics, MacKay Memorial Hospital, Taipei 10491, Taiwan
2
Holistic Education Center, Mackay Medical College, New Taipei City 252, Taiwan
3
Department of Orthopedic Surgery, Kaohsiung Chang Gung Memorial Hospital Medical Center, Kaohsiung 833, Taiwan
4
Department of Pharmacology, School of Medicine, China Medical University, Taichung 404, Taiwan
5
Chinese Medicine Research Center, China Medical University, Taichung 404, Taiwan
6
Department of Biotechnology, College of Health Science, Asia University, Taichung 413, Taiwan
7
Department of Medicine, Mackay Medical College, New Taipei City 252, Taiwan
8
Department of Internal Medicine, MacKay Memorial Hospital, Taipei 10491, Taiwan
9
Department of Education and Research, Taipei City Hospital Renai Branch, Taipei 106, Taiwan
10
Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 4 June 2018 / Revised: 1 July 2018 / Accepted: 3 July 2018 / Published: 9 July 2018
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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Abstract

Age-related bone diseases are partly caused by impaired bone integrity, which are closely related to osteoblasts’ activity and angiogenesis. Endothelial progenitor cells (EPCs) are the initiators of angiogenesis and found to have senescent-induced dysfunctions. The aim of this study is to investigate the effects of senescence in EPCs on osteogenesis and angiogenesis. Human primary EPCs and a murine osteoblast cell line (MC3T3-E1) are utilized in this study. The senescence of EPCs are induced by serial passages. When co-cultured with senescent EPCs, the osteoblasts demonstrate weakened alkaline phosphatase (ALP) activity and mineral deposition. On the other hand, osteoblast-induced migration decreases in senescent EPCs. As for the intracellular alterations of senescent EPCs, the activation of Akt/mTOR/p70S6K pathway, MnSOD and catalase are diminished. In contrast, the level of reactive oxygen species are significantly higher in senescent EPCs. Furthermore, senescent EPCs has decreased level intracellular ATP level and coupling efficiency for oxidative phosphorylation while the non-mitochondrial respiration and glycolysis are elevated. The senescence of EPCs impairs the functions of both osteoblasts and EPCs, suggesting EPCs’ role in the pathophysiology of age-related bone diseases. Targeting the alterations found in this study could be potential treatments. View Full-Text
Keywords: endothelial progenitor cell; osteoblast; senescence; Akt/mTOR/p70S6K; ATP synthesis endothelial progenitor cell; osteoblast; senescence; Akt/mTOR/p70S6K; ATP synthesis
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Wang, G.-S.; Shen, Y.-S.; Chou, W.-Y.; Tang, C.-H.; Yeh, H.-I.; Wang, L.-Y.; Yen, J.-Y.; Huang, T.-Y.; Liu, S.-C.; Yang, C.-Y.; Lin, T.-Y.; Chen, C.; Wang, S.-W. Senescence Induces Dysfunctions in Endothelial Progenitor Cells and Osteoblasts by Interfering Translational Machinery and Bioenergetic Homeostasis. Int. J. Mol. Sci. 2018, 19, 1997.

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