Zinc balance is critical for NFI‐C mediated regulation of odontoblast differentiation

Oh, Hyun‐Taek; Lee, Hye Kyung; Park, Su-Jin; Cho, Young-Sik; Bae, Hyun-Sook; Cho, Moon‐Il; Park, Joo-Cheol

doi:10.1002/jcb.23421

Cited by 20 publications

(12 citation statements)

References 46 publications

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“…Nuclear factor I‐C (NFIC) has long been believed to play an essential role in tooth formation. Disruption of the Nfic gene in mice leads to abnormal tooth roots that are predominantly caused by abnormal odontoblast differentiation and dentin formation during tooth formation (15, 16).…”

mentioning

confidence: 99%

Nuclear factor I‐C reciprocally regulates adipocyte and osteoblast differentiation via control of canonical Wnt signaling

Zhou

Wang

Qi³

et al. 2017

FASEB j.

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Nuclear factor I-C (NFIC) has recently been identified as an important player in osteogenesis and bone homeostasis However, the molecular mechanisms involved have yet to be defined. In the current study, Nfic expression was altered in primary marrow stromal cells and established progenitor lines after adipogenic and osteogenic treatment. Overexpression of Nfic in stromal cells ST2, mesenchymal cells C3H10T1/2, and primary marrow stromal cells inhibited adipogenic differentiation, whereas it promoted osteogenic differentiation. Conversely, silencing of endogenous Nfic in the cell lines enhanced adipogenic differentiation, whereas it blocked osteogenic differentiation. Mechanism investigations revealed that Nfic overexpression promoted nuclear translocation of β-catenin and increased nuclear protein levels of β-catenin and transcription factor 7-like 2 (TCF7L2). Promoter studies and the chromatin immunoprecipitation (ChIP) assay revealed that NFIC directly binds to the promoter of low-density lipoprotein receptor-related protein 5 (Lrp5) and thereafter transactivates the promoter. Finally, inactivation of canonical Wnt signaling in ST2 attenuated the inhibition of adipogenic differentiation and stimulation of osteogenic differentiation by NFIC. Our study suggests that NFIC balances adipogenic and osteogenic differentiation from progenitor cells through controlling canonical Wnt signaling and highlights the potential of NFIC as a target for new therapies to control metabolic disorders like osteoporosis and obesity.-Zhou, J., Wang, S., Qi, Q., Yang, X., Zhu, E., Yuan, H., Li, X., Liu, Y., Li, X., Wang, B. Nuclear factor I-C reciprocally regulates adipocyte and osteoblast differentiation control of canonical Wnt signaling.

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confidence: 99%

Nuclear factor I‐C reciprocally regulates adipocyte and osteoblast differentiation via control of canonical Wnt signaling

Zhou

Wang

Qi³

et al. 2017

FASEB j.

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“…ChIP assays were performed as previously described . MC3T3‐E1 cells were treated with BMP‐2 (300 ng/ml) for 48 hours.…”

Section: Methodsmentioning

confidence: 99%

NFI-C Regulates Osteoblast Differentiation via Control of Osterix Expression

et al. 2014

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In bone marrow, bone marrow stromal cells (BMSCs) have the capacity to differentiate into osteoblasts and adipocytes. Age-related osteoporosis is associated with a reciprocal decrease of osteogenesis and an increase of adipogenesis in bone marrow. In this study, we demonstrate that disruption of nuclear factor I-C (NFI-C) impairs osteoblast differentiation and bone formation, and increases bone marrow adipocytes. Interestingly, NFI-C controls postnatal bone formation but does not influence prenatal bone development. We also found decreased NFI-C expression in osteogenic cells from human osteoporotic patients. Notably, transplantation of Nfic-overexpressing BMSCs stimulates osteoblast differentiation and new bone formation, but inhibits adipocyte differentiation by suppressing peroxisome proliferator-activated receptor gamma expression in Nfic 2/2 mice showing an age-related osteoporosis-like phenotype. Finally, NFI-C directly regulates Osterix expression but acts downstream of the bone morphogenetic protein-2-Runx2 pathway. These results suggest that NFI-C acts as a transcriptional switch in cell fate determination between osteoblast and adipocyte differentiation in BMSCs. Therefore, regulation of NFI-C expression in BMSCs could be a novel therapeutic approach for treating agerelated osteoporosis.

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“…Zinc stimulates protein phosphorylation and enhances calcium deposition [Oh et al, 2012]. Zinc facilitates dentinal tubule occlusion by crystals precipitation, and these crystals do not easily dissolve after acids exposure [Gu et al, 2011].…”

Section: Discussionmentioning

confidence: 99%

Zinc Induces Apatite and Scholzite Formation during Dentin Remineralization

Osorio

Cabello

et al. 2014

Caries Res

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The aim of this study was to ascertain whether zinc may improve the repair ability of demineralized dentin. Dentin disks were demineralized by phosphoric acid during 15 s and immersed in artificial saliva, remineralizing solution, a zinc chloride solution and a zinc oxide solution. Dentin specimens were analyzed after 24 h and 1 month of storage. Surface morphology was assessed by atomic force and scanning electron microscopy, mechanical properties were analyzed by nanohardness testing in a TriboIndenter, and chemical changes at the surfaces were determined by X-ray diffraction, Raman and energy-dispersive elemental analyses. After phosphoric acid application, dentin was only partially demineralized. Demineralized dentin was remineralized after 24 h of storage in any of the tested solutions (nanohardness increased and hydroxylapatite formation was detected by Raman). Remineralization was maintained up to 1 month in dentin stored in remineralizing solution, zinc chloride and zinc oxide. Zinc and phosphate were important for hydroxylapatite homeostasis. Scholzite formation was encountered in dentin stored in zinc-containing solutions. Zinc might allow to reach the balance between dentin demineralization and remineralization processes.

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Zinc balance is critical for NFI‐C mediated regulation of odontoblast differentiation

Cited by 20 publications

References 46 publications

Nuclear factor I‐C reciprocally regulates adipocyte and osteoblast differentiation via control of canonical Wnt signaling

Nuclear factor I‐C reciprocally regulates adipocyte and osteoblast differentiation via control of canonical Wnt signaling

NFI-C Regulates Osteoblast Differentiation via Control of Osterix Expression

Zinc Induces Apatite and Scholzite Formation during Dentin Remineralization

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