Epigenetic regulation of Runx2 transcription and osteoblast differentiation by nicotinamide phosphoribosyltransferase

Liu, Min; Huang, Peixin; Islam, Shamima; Heruth, Daniel P.; Li, Xuanan; Zhang, Li Qin; Li, Ding‐You; Hu, Zhaohui; Ye, Shui Qing

doi:10.1186/s13578-017-0154-6

Cited by 47 publications

(36 citation statements)

References 34 publications

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“…However, recombinant NAMPT protein did not regulate MMP‐2, MMP‐9, MMP‐13, or RANKL/OPG mRNA expression in osteoblast cultures. Moreover, NAMPT only regulated BSP and OC expression, whereas it has been recently shown that NAMPT promotes increased function of Runx2 in osteoblast cultures (Ling et al, ). We used a mature osteoblast cell culture in which matrix production and mineralization were activated.…”

Section: Discussionmentioning

confidence: 99%

NAMPT expression in osteoblasts controls osteoclast recruitment in alveolar bone remodeling

Hassan

Baroukh

Llorens

et al. 2018

Journal Cellular Physiology

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In bone remodeling, osteoclasts are recruited via increased production of RANKL (receptor activator of nuclear factor-κB ligand) and migrate to the bone surface, aided by matrix metalloproteinases (MMPs). NAMPT (nicotinamide phosphoribosyl transferase), which catalyzes the rate-limiting step in the NAD salvage pathway, increases during in vitro osteogenic differentiation and inhibits RANKL-induced osteoclast differentiation. Alveolar bone loss, due to disturbance of the remodeling process, is a major feature of periodontitis. Thus, we investigated the role of NAMPT in a synchronized alveolar bone remodeling rat model. NAMPT expression increased in osteogenic cells during the remodeling activation phase, in parallel with RANKL and MMP-2 expression. Inhibition of NAMPT activity, by systemic delivery of its selective inhibitor FK866, decreased the recruitment of osteoclasts, but not their activity. In vitro, NAMPT mRNA, and protein expression also increased during osteoblast differentiation in primary calvarial osteoblast cultures. Recombinant NAMPT and NMN, its direct metabolite, dose-dependently increased bone marker expression, including that of sialoprotein (BSP) and osteocalcin (OC), whereas their expression was inhibited by FK866 treatment. Recombinant NAMPT did not regulate MMP-2, -9, MMP-13, or RANKL/OPG mRNA expression in osteoblasts. Our data suggest that de novo NAMPT synthesis in osteoblasts controls cell differentiation through osteoclast recruitment during the activation of bone remodeling.

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Section: Discussionmentioning

confidence: 99%

NAMPT expression in osteoblasts controls osteoclast recruitment in alveolar bone remodeling

Hassan

Baroukh

Llorens

et al. 2018

Journal Cellular Physiology

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“…Further, Shen et al found an increased level of acetylation at H3 and H4 histones near the promoter region of OC gene during osteoblastic differentiation of BMSCs, hence, reported an absolute association between core histone and OC gene expression [98]. Apart from these, nicotinamide phosphoribosyltransferase (Nampt), absent, small, or homeotic disc1 like (Ash1l) and CCAAT/enhancer-binding protein beta (CEBPB) have also been reported to play important roles in augmenting osteogenic differentiation of BMSCs [102][103][104]. MicroRNAs being epigenetic regulators also play their roles during osteogenic differentiation of BMSCs.…”

Section: Epigenetic Factors Involved In Osteogenic Differentiation Ofmentioning

confidence: 99%

Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

Qadir

Liang

et al. 2020

IJMS

156

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Senile osteoporosis has become a worldwide bone disease with the aging of the world population. It increases the risk of bone fracture and seriously affects human health. Unlike postmenopausal osteoporosis which is linked to menopause in women, senile osteoporosis is due to aging, hence, affecting both men and women. It is commonly found in people with more than their 70s. Evidence has shown that with age increase, bone marrow stromal cells (BMSCs) differentiate into more adipocytes rather than osteoblasts and undergo senescence, which leads to decreased bone formation and contributes to senile osteoporosis. Therefore, it is necessary to uncover the molecular mechanisms underlying the functional changes of BMSCs. It will benefit not only for understanding the senile osteoporosis development, but also for finding new therapies to treat senile osteoporosis. Here, we review the recent advances of the functional alterations of BMSCs and the related mechanisms during senile osteoporosis development. Moreover, the treatment of senile osteoporosis by aiming at BMSCs is introduced.

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“…In order to determine whether these contradicting results may have been due to use of different cell types, and to determine the effects of FGF18 on osteogenic differentiation, the present study investigated the effect of FGF18 on the viability and differentiation of MC3T3-E1 cells and the potential underlying mechanisms involved. The MC3T3-E1 cell line possesses the ability to self-renew and differentiate into osteoblasts, and is used as a model to study the osteogenic process in vitro (22,23).…”

Section: Introductionmentioning

confidence: 99%

FGF18 inhibits MC3T3-E1 cell osteogenic differentiation via the ERK signaling pathway

Zhai

Song

et al. 2017

Molecular Medicine Reports

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Fibroblast growth factor (FGF) 18 is a member of the FGF family and serves a key role in skeletal growth and development. The present study investigated the effect of FGF18 on pre‑osteoblast MC3T3-E1 cells and the signaling pathways involved by performing an alkaline phosphatase (ALP) assay and reverse transcription‑quantitative polymerase chain reaction. MC3T3‑E1 cells incubated in a culture medium supplemented with FGF18 exhibited increased viability when compared with the untreated control cells. In addition, ALP activity was decreased in MC3T3‑E1 cells treated with FGF18 plus an osteogenic medium (OM) for 7 and 14 days when compared with untreated and OM‑treated controls. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) results demonstrated that the expression of osteoblastic‑associated genes was significantly repressed in FGF18 plus OM‑treated MC3T3‑E1 cells, including ALP, collagen type I, osteocalcin, bone sialo protein and osterix. These results suggested that the expression levels of genes associated with osteogenesis were mainly repressed. In addition, combined treatment of MC3T3‑E1 cells with OM and FGF18 led to a significant reduction in mineral deposition when compared with the OM‑only treated group. Furthermore, FGF18 activated the extracellular signal‑regulated kinase pathway in MC3T3‑E1 cells, which may have been responsible for the observed decrease in the expression of osteoblastic‑associated genes. In conclusion, the results suggest that FGF18 may be involved in MC3T3‑E1 cell proliferation and osteoblastic differentiation.

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Epigenetic regulation of Runx2 transcription and osteoblast differentiation by nicotinamide phosphoribosyltransferase

Cited by 47 publications

References 34 publications

NAMPT expression in osteoblasts controls osteoclast recruitment in alveolar bone remodeling

NAMPT expression in osteoblasts controls osteoclast recruitment in alveolar bone remodeling

Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

FGF18 inhibits MC3T3-E1 cell osteogenic differentiation via the ERK signaling pathway

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