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      Nicotinamide mononucleotide attenuates glucocorticoid-induced osteogenic inhibition by regulating the SIRT1/PGC-1α signaling pathway

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          Abstract

          Long-term and high-dose glucocorticoid treatment is recognized as an important influencing factor for osteoporosis and osteonecrosis. Nicotinamide mononucleotide (NMN) is an intermediate of NAD + biosynthesis, and is widely used to replenish the levels of NAD +. However, the potential role of NMN in glucocorticoid-induced osteogenic inhibition remains to be demonstrated. In the present study, the protective effects of NMN on dexamethasone (Dex)-induced osteogenic inhibition, and its underlying mechanisms, were investigated. Bone mesenchymal stem cells were treated with Dex, which decreased the levels of the osteogenic markers alkaline phosphatase, Runt-related transcription factor 2 and osteocalcin. NMN treatment attenuated Dex-induced osteogenic inhibition and promoted the expression of sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α. SIRT1 knockdown reversed the protective effects of NMN and reduced the expression levels of PGC-1α. Collectively, the results of the present study reveal that NMN may be a potential therapeutic target for glucocorticoid-induced osteoporosis.

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          Mammalian sirtuins--emerging roles in physiology, aging, and calorie restriction.

          Marcia Haigis, Leonard Guarente (2006)
          Sir2 is an NAD-dependent deacetylase that connects metabolism with longevity in yeast, worms and flies. Mammals contain seven homologs of yeast Sir2, SIRT1-7. Here, we review recent findings demonstrating the role of these mammalian sirtuins as regulators of physiology, calorie restriction, and aging. The current findings sharpen our understanding of sirtuins as potential pharmacological targets to treat the major diseases of aging.
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            Sirtuin 1 and sirtuin 3: physiological modulators of metabolism.

            Rubén Nogueiras, Kirk M. Habegger, Nilika Chaudhary … (2012)
            The sirtuins are a family of highly conserved NAD(+)-dependent deacetylases that act as cellular sensors to detect energy availability and modulate metabolic processes. Two sirtuins that are central to the control of metabolic processes are mammalian sirtuin 1 (SIRT1) and sirtuin 3 (SIRT3), which are localized to the nucleus and mitochondria, respectively. Both are activated by high NAD(+) levels, a condition caused by low cellular energy status. By deacetylating a variety of proteins that induce catabolic processes while inhibiting anabolic processes, SIRT1 and SIRT3 coordinately increase cellular energy stores and ultimately maintain cellular energy homeostasis. Defects in the pathways controlled by SIRT1 and SIRT3 are known to result in various metabolic disorders. Consequently, activation of sirtuins by genetic or pharmacological means can elicit multiple metabolic benefits that protect mice from diet-induced obesity, type 2 diabetes, and nonalcoholic fatty liver disease.
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              Osteogenesis and aging: lessons from mesenchymal stem cells

              Arantza Infante, Clara I Rodríguez (2018)
              Aging is a high risk factor for the development of osteoporosis, a multifactorial age-related progressive disease characterized by reduced bone mass and increased risk of fractures. At the cellular level, the mesenchymal stem cell pool in the bone marrow niche shows a biased differentiation into adipogenesis at the cost of osteogenesis. This differentiation shift leads to decreased bone formation, contributing to the etiology of osteoporosis. This review will focus on the most recent/relevant molecular findings driving this functional impairment of mesenchymal stem cells in the aging process.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Med Rep
                Journal ID (iso-abbrev): Mol Med Rep
                Title: Molecular Medicine Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 1791-2997
                ISSN (Electronic): 1791-3004
                Publication date (Print): July 2020
                Publication date (Electronic): 04 May 2020
                Publication date PMC-release: 04 May 2020
                Volume: 22
                Issue: 1
                Pages: 145-154
                Affiliations
                [1 ]Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330000, P.R. China
                [2 ]Department of Orthopedics, Gao'an People's Hospital, Gao'an, Jiangxi 330800, P.R. China
                Author notes
                Correspondence to: Professor Jun Tao, Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Donghu, Nanchang, Jiangxi 330000, P.R. China, E-mail: 2431835455@ 123456qq.com
                Article
                Publisher ID: MMR-22-01-145
                DOI: 10.3892/mmr.2020.11116
                PMC ID: 7248519
                PubMed ID: 32377728
                SO-VID: 2c112950-9002-4638-ba33-14bf5a99b2f5
                Copyright © Copyright: © Huang et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 19 August 2019
                Date accepted : 03 March 2020
                Categories
                Subject: Articles

                Keywords: nicotinamide mononucleotide,osteoporosis,sirtuin 1,peroxisome proliferator-activated receptor gamma coactivator
                Data availability:
                Keywords: nicotinamide mononucleotide, osteoporosis, sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator

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