Journal article
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Arginase-ii deficiency extends lifespan in mice
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Xiong, Yuyan
Division of Physiology, Cardiovascular and Aging Research, Department of Medicine, University of Fribourg, Switzerland
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Yepuri, Gautham
Division of Physiology, Cardiovascular and Aging Research, Department of Medicine, University of Fribourg, Switzerland
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Montani, Jean-Pierre
Division of Physiology, Cardiovascular and Aging Research, Department of Medicine, University of Fribourg, Switzerland - National Center of Competence in Research “Kidney.CH”, Fribourg, Switzerland
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Ming, Xiu-Fen
Division of Physiology, Cardiovascular and Aging Research, Department of Medicine, University of Fribourg, Switzerland - National Center of Competence in Research “Kidney.CH”, Fribourg, Switzerland
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Yang, Zhihong
Division of Physiology, Cardiovascular and Aging Research, Department of Medicine, University of Fribourg, Switzerland - National Center of Competence in Research “Kidney.CH”, Fribourg, Switzerland
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Published in:
- Frontiers in Physiology. - 2017, vol. 8, p. 682
English
The mitochondrial arginase type II (Arg-II) has been shown to interact with ribosomal protein S6 kinase 1 (S6K1) and mitochondrial p66Shc and to promote cell senescence, apoptosis and inflammation under pathological conditions. However, the impact of Arg-II on organismal lifespan is not known. In this study, we demonstrate a significant lifespan extension in mice with Arg-II gene deficiency (Arg-II-/-) as compared to wild type (WT) control animals. This effect is more pronounced in the females than in the males. The gender difference is associated with higher Arg-II expression levels in the females than in the males in skin and heart at both young and old age. Ablation of Arg-II gene significantly reduces the aging marker p16INK4a levels in these tissues of old female mice, whereas in the male mice this effect of Arg- II deficiency is weaker. In line with this observation, age-associated increases in S6K1 signaling and p66Shc levels in heart are significantly attenuated in the female Arg-II-/- mice. In the male mice, only p66Shc but not S6K1 signaling is reduced. In summary, our study demonstrates that Arg-II may play an important role in the acceleration of aging in mice. Genetic disruption of Arg-II in mouse extends lifespan predominantly in females, which relates to inhibition of S6K1, p66Shc, and p16INK4a. Thus, Arg-II may represent a promising target to decelerate aging process and extend lifespan as well as to treat age-related diseases.
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Faculty
- Faculté des sciences et de médecine
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Department
- Département de Médecine
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Language
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Classification
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Biological sciences
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License
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License undefined
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Identifiers
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Persistent URL
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https://folia.unifr.ch/unifr/documents/306049
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