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

2012 ◽  
Vol 113 (3) ◽  
pp. 877-887 ◽  
Author(s):  
Hyun-Jung Oh ◽  
Hye-Kyung Lee ◽  
Su-Jin Park ◽  
Young-Sik Cho ◽  
Hyun-Sook Bae ◽  
...  
Keyword(s):  
Odontoblast Differentiation ◽  
Zinc Balance

LncRNA DANCR sponges miR-216a to inhibit odontoblast differentiation through upregulating c-Cbl

2020 ◽  
Vol 387 (1) ◽  
pp. 111751
Author(s):  
Lingling Chen ◽  
Zhi Song ◽  
Jinyan Wu ◽  
Qiting Huang ◽  
Zongshan Shen ◽  
...  
Keyword(s):  
Odontoblast Differentiation

scholarly journals Microtubule-associated Protein 1b, a Neuronal Marker Involved in Odontoblast Differentiation

2009 ◽  
Vol 35 (7) ◽  
pp. 992-996 ◽  
Author(s):  
Jean-Christophe Maurin ◽  
Marie-Lise Couble ◽  
Marie-Jeanne Staquet ◽  
Florence Carrouel ◽  
Imad About ◽  
...  
Keyword(s):  
Neuronal Marker ◽  
Odontoblast Differentiation

Suberoylanilide Hydroxamic Acid Enhances Odontoblast Differentiation

2012 ◽  
Vol 91 (5) ◽  
pp. 506-512 ◽  
Author(s):  
A. Kwon ◽  
H.-J. Park ◽  
K. Baek ◽  
H.-L. Lee ◽  
J.-C. Park ◽  
...  
Keyword(s):  
Hydroxamic Acid ◽  
Suberoylanilide Hydroxamic Acid ◽  
Odontoblast Differentiation

scholarly journals Hypoxia-inducible factor 1α induces osteo/odontoblast differentiation of human dental pulp stem cells via Wnt/β-catenin transcriptional cofactor BCL9

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Shion Orikasa ◽  
Nobuyuki Kawashima ◽  
Kento Tazawa ◽  
Kentaro Hashimoto ◽  
Keisuke Sunada-Nara ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dental Pulp ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Dental Pulp Stem Cells ◽  
Pulp Tissue ◽  
Odontoblast Differentiation ◽  
Hypoxia Inducible Factor 1Α ◽  
Hypoxic Conditions

AbstractAccelerated dental pulp mineralization is a common complication in avulsed/luxated teeth, although the mechanisms underlying this remain unclear. We hypothesized that hypoxia due to vascular severance may induce osteo/odontoblast differentiation of dental pulp stem cells (DPSCs). This study examined the role of B-cell CLL/lymphoma 9 (BCL9), which is downstream of hypoxia-inducible factor 1α (HIF1α) and a Wnt/β-catenin transcriptional cofactor, in the osteo/odontoblastic differentiation of human DPSCs (hDPSCs) under hypoxic conditions. hDPSCs were isolated from extracted healthy wisdom teeth. Hypoxic conditions and HIF1α overexpression induced significant upregulation of mRNAs for osteo/odontoblast markers (RUNX2, ALP, OC), BCL9, and Wnt/β-catenin signaling target genes (AXIN2, TCF1) in hDPSCs. Overexpression and suppression of BCL9 in hDPSCs up- and downregulated, respectively, the mRNAs for AXIN2, TCF1, and the osteo/odontoblast markers. Hypoxic-cultured mouse pulp tissue explants showed the promotion of HIF1α, BCL9, and β-catenin expression and BCL9-β-catenin co-localization. In addition, BCL9 formed a complex with β-catenin in hDPSCs in vitro. This study demonstrated that hypoxia/HIF1α-induced osteo/odontoblast differentiation of hDPSCs was partially dependent on Wnt/β-catenin signaling, where BCL9 acted as a key mediator between HIF1α and Wnt/β-catenin signaling. These findings may reveal part of the mechanisms of dental pulp mineralization after traumatic dental injury.

scholarly journals Lithium Chloride Exerts Differential Effects on Dentinogenesis and Osteogenesis in Primary Pulp Cultures

2021 ◽  
Vol 2 ◽  
Author(s):  
Anushree Vijaykumar ◽  
Mina Mina
Keyword(s):  
Dental Pulp ◽  
Osteoblast Differentiation ◽  
Prolonged Treatment ◽  
Odontoblast Differentiation ◽  
Positive Effects ◽  
Reparative Dentin ◽  
Dentin Formation ◽  
Reparative Dentin Formation

Wnt/β-catenin signaling is known to play essential roles in odontoblast differentiation and reparative dentin formation. Various Wnt activators including LiCl have been increasingly studied for their effectiveness to induce repair of the dentin-pulp complex. LiCl is a simple salt thought to activate Wnt/β-catenin signaling by inhibiting GSK3β. Previous in vitro and in vivo studies showed that LiCl increased odontoblast differentiation and enhanced reparative dentin formation. However, the underlying molecular and cellular mechanisms by which LiCl regulates odontoblast and osteoblast differentiation during reparative dentinogenesis are not well-understood. Our in vitro studies show that exposure of early dental pulp progenitors to LiCl increased the survival and the pool of αSMA+ progenitors, leading to enhanced odontoblast and osteoblast differentiation. The positive effects of LiCl in the differentiation of osteoblasts and odontoblasts from αSMA+ progenitors are mediated by Wnt/β-catenin signaling. Our results also showed that continuous and late exposure of dental pulp cells to LiCl increased the expression of odontoblast markers through Wnt/β-catenin signaling, and the number of odontoblasts expressing DMP1-Cherry and DSPP-Cerulean transgenes. However, unlike the early treatment, both continuous and late treatments decreased the expression of Bsp and the expression of BSP-GFPtpz transgene. These observations suggest that prolonged treatment with LiCl in more mature cells of the dental pulp has an inhibitory effect on osteoblast differentiation. The inhibitory effects of LiCl on osteogenesis and Bsp were not mediated through Wnt/β-catenin signaling. These observations suggest that the effects of LiCl, and GSK3β antagonists on reparative dentinogenesis involve multiple pathways and are not specific to Wnt/β-catenin signaling.

Changes in plasma zinc content after exercise in men fed a low-zinc diet

1984 ◽  
Vol 247 (1) ◽  
pp. E88-E93 ◽  
Author(s):  
H. C. Lukaski ◽  
W. W. Bolonchuk ◽  
L. M. Klevay ◽  
D. B. Milne ◽  
H. H. Sandstead
Keyword(s):  
Copper Content ◽  
Maximal Exercise ◽  
Strong Predictor ◽  
Zinc Content ◽  
Plasma Zinc ◽  
Zinc Depletion ◽  
Plasma Copper ◽  
Zinc Concentrations ◽  
Zinc Repletion ◽  
Zinc Balance

For 30 days five healthy men aged 23-57 yr consumed a diet adequate in zinc (8.6 mg/day); they ate a low-zinc diet (3.6 mg/day) for the next 120 days and then received a zinc-supplemented (33.6 mg/day) diet for 30 days. Copper intake was constant at 1.8 mg/day. Aerobic capacity was determined periodically during each diet period. Relative zinc balance (% of control) declined during depletion (r = -0.28, P less than 0.009). Pre- and postexercise zinc concentrations decreased when dietary zinc was restricted (r = -0.61, P less than 0.0001 and r = -0.78, P less than 0.0001) and increased with supplementation (r = 0.61, P less than 0.008 and r = 0.76, P less than 0.0003, respectively). Both plasma zinc and hematocrit increased (P less than 0.01) after maximal exercise. To minimize the effect of hemoconcentration during exercise, the van Beaumont quotient (J. Appl. Physiol. 34: 102-106, 1973) was calculated using pre- and postexercise hematocrit and plasma zinc. The initial quotient of 1.8 +/- 1.8% (mean +/- SE) declined (P less than 0.05) to -7.4 +/- 2.3% during depletion. With zinc repletion, the quotient increased to 6.9 +/- 3.6%, which was greater (P less than 0.05) than the quotient in depletion but similar to the initial quotient. The quotient was a strong predictor (r = 0.71, P less than 0.0005) of the change in relative zinc balance during zinc depletion. In contrast, no changes were found in plasma copper content. These data suggest that zinc mobilization from tissues is impaired during zinc depletion, and they validate the use of the van Beaumont quotient as an index of change in body zinc stores.

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