Expression of Notch signalling‐related genes in normal and differentiating rat dental pulp cells

Sun, Han; Kawashima, Nobuyuki; Xu, Jing; Takahashi, Satoshi; Suda, Hiroshi

doi:10.1111/j.1747-4477.2009.00188.x

Cited by 6 publications

(5 citation statements)

References 31 publications

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“…The other growth factors involved in odontoblast differentiation include epidermal growth factor (Liang et al ; Liang et al ), FGF2 (Nakao et al ; Shimabukuro et al ; Morito et al ; Shimabukuro et al ), growth differentiation factor 11 (Nakashima et al ; Nakashima et al ), platelet‐derived growth factor (PDGF) (Yokose et al ), hepatocyte growth factor (Li et al ), and insulin‐like growth factors (IGF) (Onishi et al ). Odontoblast differentiation is modulated by various molecules, including twist (Galler et al ), Nuclear factor I‐C (Lee et al ), Notch (Zhang et al ; Sun et al ), Wnt (Scheller et al ; Koizumi et al ), Runx2, Sp7 (Chen et al ), Runx3 (Zheng et al ), and DLX3 (Choi et al ). However, the specific factor(s) or gene(s), including master genes, required for commitment to odontoblast differentiation remain unclear.…”

Section: Morphology and Development Of Odontoblastsmentioning

confidence: 99%

“…For example, MEPE (Wang et al ; Wang et al ) and periostin (Zhou et al ) negatively regulate the expression of odontoblastic markers. In addition, Notch is a receptor that is involved in the development of various tissues/cells and has negative effects on both osteoblast differentiation (Shindo et al ) and odontoblast differentiation (Sun et al ). Controlling odontoblast differentiation is key to the induction of pulp tissue regeneration.…”

Section: Odontoblast Precursors Dpsc and Pulp Regenerationmentioning

confidence: 99%

“…), Nuclear factor I-C(Lee et al 2009), Notch(Zhang et al 2008;Sun et al 2010), Wnt(Scheller et al 2008;Koizumi et al 2013), Runx2, Sp7(Chen et al 2009), Runx3(Zheng et al 2007), and DLX3(Choi et al 2010). …”

mentioning

confidence: 99%

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Odontoblasts: Specialized hard‐tissue‐forming cells in the dentin‐pulp complex

Kawashima

Okiji

2016

Congenital Anomalies

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134

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Odontoblasts are specialized cells that produce dentin and exhibit unique morphological characteristics; i.e., they extend cytoplasmic processes into dentinal tubules. While osteoblasts, which are typical hard-tissue-forming cells, are generated from mesenchymal stem cells during normal and pathological bone metabolism, the induction of odontoblasts only occurs once during tooth development, and odontoblasts survive throughout the lives of healthy teeth. During the differentiation of odontoblasts, signaling molecules from the inner enamel epithelium are considered necessary for the differentiation of odontoblast precursors, i.e., peripheral dental papilla cells. If odontoblasts are destroyed by severe external stimuli, such as deep caries, the differentiation of dental pulp stem cells into odontoblast-like cells is induced. Various bioactive molecules, such as non-collagenous proteins, might be involved in this process, although the precise mechanisms responsible for odontoblast differentiation have not been fully elucidated. Recently, our knowledge about the other functional activities of odontoblasts (apart from dentin formation) has increased. For example, it has been suggested that odontoblasts might act as nociceptive receptors, and surveillance cells that detect the invasion of exogenous pathogens. The regeneration of the dentin-pulp complex has recently gained much attention as a promising future treatment modality that could increase the longevity of pulpless teeth. Finally, congenital dentin anomalies, which are concerned with the disturbance of odontoblast functions, are summarized.

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Section: Morphology and Development Of Odontoblastsmentioning

confidence: 99%

Section: Odontoblast Precursors Dpsc and Pulp Regenerationmentioning

confidence: 99%

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Odontoblasts: Specialized hard‐tissue‐forming cells in the dentin‐pulp complex

Kawashima

Okiji

2016

Congenital Anomalies

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134

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“…Numerous studies have demonstrated that Hey1 is responsible for the development of various tissues, including bone, nerve, heart, muscle and vascular tissues ( 17 – 21 ). Our preliminary study demonstrated that Hey1 was expressed in dental pulp tissues and may affect dentin sialophosphoprotein (DSPP) expression during odontogenesis ( 22 ). In addition, substantial evidence has demonstrated the regulatory roles of Hey1 in mineralization ( 23 , 24 ).…”

Section: Introductionmentioning

confidence: 99%

Hey1 functions as a positive regulator of odontogenic differentiation in odontoblast‑lineage cells

et al. 2017

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Substantial evidence has indicated that Notch and bone morphogenetic protein (BMP) signaling may regulate odontoblastic differentiation. Hairy/enhancer-of-split related with YRPW motif 1 (Hey1), a downstream target gene of Notch and BMP signaling, is expressed in dental pulp tissues and has been demonstrated to be responsible for osteoblast mineralization. The aim of this study was to investigate the effects of Hey1 on odontoblast differentiation. The results of the study demonstrated that Hey1 expression in odontoblast-lineage cells (OLCs) was upregulated by stimulation of osteoblastic/odontoblastic differentiation medium containing ascorbic acid, β-glycerol phosphate and dexamethasone. Furthermore, stable Hey1-overexpressing cells expressed higher levels of dentin sialophosphoprotein (DSPP) and exhibited higher mineralization capabilities following stimulation by differentiation medium. Furthermore, RNA interference-mediated knockdown of Hey1 downregulated the expression levels of DSPP in OLCs stimulated by differentiation medium. Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation. The present study broadens the understanding of odontoblast differentiation and biomineralization.

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“…Dexamethasone interacted with BMP2 then regulated osteogenic differentiation in human MSC (Jager et al, 2008). Dexamethasone regulated Notch target gene expression in rat dental pulp cells (Sun et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Dorsomorphin attenuates Jagged1‐induced mineralization in human dental pulp cells

et al. 2021

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Aim To investigate whether TGF‐β/BMP signalling participates in Jagged1‐induced osteogenic differentiation in human dental pulp cells (hDPs). Methodology Bioinformatic analysis of publicly available RNA sequencing data of Jagged1‐treated hDPs was performed using NetworkAnalyst. The mRNA expression was validated using real‐time polymerase chain reaction. hDPs were seeded on Jagged1 immobilized surfaces in the presence or absence of TGF‐β or BMP inhibitor. Osteogenic differentiation was evaluated using alkaline phosphatase staining, osteogenic marker gene expression and mineralization assay. Statistical analyses were performed using a Kruskal–Wallis test, followed by a pairwise comparison for more than three group comparison. Mann–Whitney U‐test was employed for two group comparison. The statistical significance was considered at p < .05. Results Jagged1 treatment in growth medium significantly promoted TGFB1, TGFB2 and TGFB3 whilst significantly inhibited BMP2, BMP4 and BMP6 mRNA expression (p < .05). In osteogenic induction medium, Jagged1 significantly up‐regulated TGFB1, TGFB2 and TGFB3 at days 1 and 3 (p < .05). Pre‐treatment with TGF‐β1, TGF‐β2 or TGF‐β3 prior to osteogenic induction resulted in the significant increase of osteogenic marker gene expression, collagen type 1 protein expression, alkaline phosphatase enzymatic activity and mineral deposition (p < .05). However, TGF‐β signalling inhibition with SB431542 (4 μmol L−1) or SB505124 (47 and 129 nmol L−1) failed to attenuate the effect of Jagged1‐induced osteogenic differentiation in hDPs. Dorsomorphin (4 and 8 μmol L−1) treatment significantly abolished the effect of Jagged1 on mineralization by hDPs (p < .05). Conclusion Notch signalling activation by Jagged1 modulated TGF‐β and BMP ligand expression. Dorsomorphin, but not TGF‐β receptor inhibitor, attenuated Jagged1‐induced osteogenic differentiation in hDPs.

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Expression of Notch signalling‐related genes in normal and differentiating rat dental pulp cells

Cited by 6 publications

References 31 publications

Odontoblasts: Specialized hard‐tissue‐forming cells in the dentin‐pulp complex

Odontoblasts: Specialized hard‐tissue‐forming cells in the dentin‐pulp complex

Hey1 functions as a positive regulator of odontogenic differentiation in odontoblast‑lineage cells

Dorsomorphin attenuates Jagged1‐induced mineralization in human dental pulp cells

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