scholarly journals Runx3 negatively regulates Osterix expression in dental pulp cells

2007 ◽  
Vol 405 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Li Zheng ◽  
Koichiro Iohara ◽  
Masaki Ishikawa ◽  
Takeshi Into ◽  
Teruko Takano-Yamamoto ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Dental Pulp ◽  
Tooth Development ◽  
Tooth Germ ◽  
Dental Pulp Cells ◽  
Mobility Shift ◽  
Pulp Cells ◽  
Mobility Shift Assay ◽  
Responsive Element

Osterix, a zinc-finger-containing transcription factor, is required for osteoblast differentiation and bone formation. Osterix is also expressed in dental mesenchymal cells of the tooth germ. However, transcriptional regulation by Osterix in tooth development is not clear. Genetic studies in osteogenesis place Osterix downstream of Runx2 (Runt-related 2). The expression of Osterix in odontoblasts overlaps with Runx3 during terminal differentiation in vivo. Runx3 down-regulates Osterix expression in mouse DPCs (dental pulp cells). Therefore the regulatory role of Runx3 on Osterix expression in tooth development was investigated. Enforced expression of Runx3 down-regulated the activity of the Osterix promoter in the human embryonic kidney 293 cell line. When the Runx3 responsive element on the Osterix promoter, located at −713 to −707 bp (site 3, AGTGGTT) relative to the cap site, was mutated, this down-regulation was abrogated. Furthermore, electrophoretic mobility-shift assay and chromatin immunoprecipitation assays in mouse DPCs demonstrated direct functional binding of Runx3 to the Osterix promoter. These results demonstrate the transcriptional regulation of Osterix expression by Runx3 during differentiation of dental pulp cells into odontoblasts during tooth development.

TheHOX genes are expressed, in vivo, in human tooth germs: In vitro cAMP exposure of dental pulp cells results in parallel HOX network activation and neuronal differentiation

2006 ◽  
Vol 97 (4) ◽  
pp. 836-848 ◽  
Author(s):  
Vincenzo D'Antò ◽  
Monica Cantile ◽  
Maria D'Armiento ◽  
Giulia Schiavo ◽  
Gianrico Spagnuolo ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Dental Pulp ◽  
Human Tooth ◽  
Dental Pulp Cells ◽  
Network Activation ◽  
Pulp Cells ◽  
Tooth Germs

The location and characteristics of two populations of dental pulp cells affect tooth development

2009 ◽  
Vol 117 (2) ◽  
pp. 113-121 ◽  
Author(s):  
Yoshinori Sumita ◽  
Shuhei Tsuchiya ◽  
Izumi Asahina ◽  
Hideaki Kagami ◽  
Masaki J. Honda
Keyword(s):  
Dental Pulp ◽  
Tooth Development ◽  
Dental Pulp Cells ◽  
Pulp Cells ◽  
Two Populations

scholarly journals Visfatin Induces Senescence of Human Dental Pulp Cells

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 193 ◽  
Author(s):  
Chang Youp Ok ◽  
Sera Park ◽  
Hye-Ock Jang ◽  
Takashi Takata ◽  
Moon-Kyoung Bae ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Human Dental Pulp ◽  
Pulp Cells ◽  
Secretory Phenotype ◽  
Interfering Rna ◽  
First Time

Dental pulp plays an important role in the health of teeth. The aging of teeth is strongly related to the senescence of dental pulp cells. A novel adipokine, visfatin, is closely associated with cellular senescence. However, little is known about the effect of visfatin on the senescence of human dental pulp cells (hDPCs). Here, it was found that in vivo visfatin levels in human dental pulp tissues increase with age and are upregulated in vitro in hDPCs during premature senescence activated by H2O2, suggesting a correlation between visfatin and senescence. In addition, visfatin knockdown by small interfering RNA led to the reduction in hDPC senescence; however, treatment with exogenous visfatin protein induced the senescence of hDPCs along with increased NADPH consumption, which was reversed by FK866, a chemical inhibitor of visfatin. Furthermore, visfatin-induced senescence was associated with both the induction of telomere damage and the upregulation of senescence-associated secretory phenotype (SASP) factors as well as NF-κB activation, which were all inhibited by FK866. Taken together, these results demonstrate, for the first time, that visfatin plays a pivotal role in hDPC senescence in association with telomere dysfunction and the induction of SASP factors.

Effect of cleidocranial dysplasia-related novel mutation of RUNX2 on characteristics of dental pulp cells and tooth development

2010 ◽  
Vol 111 (6) ◽  
pp. 1473-1481 ◽  
Author(s):  
DongYing Xuan ◽  
Xi Sun ◽  
YuXia Yan ◽  
BaoYi Xie ◽  
PingPing Xu ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Tooth Development ◽  
Novel Mutation ◽  
Cleidocranial Dysplasia ◽  
Dental Pulp Cells ◽  
Pulp Cells

Preparation and characterization of Jagged1-bound fibrinogen-based microspheres and their cytotoxicity against human dental pulp cells

2020 ◽  
Vol 34 (8) ◽  
pp. 1105-1113
Author(s):  
Chawan Manaspon ◽  
Lawan Boonprakong ◽  
Thantrira Porntaveetus ◽  
Thanaphum Osathanon
Keyword(s):  
Dental Pulp ◽  
Biomedical Application ◽  
Binding Capacity ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Significant Difference ◽  
Human Dental Pulp ◽  
Pulp Cells

Surface immobilization of Jagged1 promotes odonto/osteogenic differentiation in human dental pulp cells. On the contrary, soluble Jagged1 fails to activate target gene expression of Notch signaling which is important for differentiation of human dental pulp cells. Hence, Jagged1 delivery system is indeed required for transportation of immobilized Jagged1 to promote odontogenic differentiation of human dental pulp cells in vivo. The present study described the preparation and characterization of Jagged1-bound fibrinogen-based microspheres. Water-in-oil emulsion technique was employed to prepare fibrinogen microspheres and thrombin cross-linked fibrinogen microspheres. The average size of fibrinogen microspheres and thrombin cross-linked fibrinogen microspheres was 213.9 ± 35.9 and 199.9 ± 41.9 µm, respectively. These microspheres did not alter the human dental pulp cells’ cell viability. Human dental pulp cells were able to attach and spread on these microspheres. Jagged1 was conjugated on microspheres using 1-ethyl-3-(3-dimethylamino) propyl carbodiimide/N-hydroxysuccinimide. Binding capacity of Jagged1 on both fibrinogen microspheres and thrombin cross-linked fibrinogen microspheres ranged from 25.8 ± 6.0 to 35.6 ± 9.1%. There was no significant difference in the size of microspheres between before and after Jagged1 conjugation process. In conclusion, fibrinogen microspheres and thrombin cross-linked fibrinogen microspheres could be utilized as the alternative biomaterials for Jagged1 delivery for future biomedical application.

scholarly journals SAT-450 Essential Role of GATA2 in the Negative Regulation of the Prepro-Thyrotropin-Releasing Hormone Gene by Liganded T3 in the Rat Paraventricular Nucleus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Go Kuroda ◽  
Shigekazu Sasaki ◽  
Akio Matsushita ◽  
Kenji Ohba ◽  
Yuki Sakai ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Paraventricular Nucleus ◽  
Negative Regulation ◽  
Thyrotropin Releasing Hormone ◽  
Mobility Shift ◽  
Releasing Hormone ◽  
Melanocortin 4 Receptor ◽  
Mobility Shift Assay ◽  
Responsive Element

Abstract T3 inhibits thyrotropin-releasing hormone (TRH) synthesis in hypothalamic paraventricular nucleus (PVN). Although T3 receptor (TR) β2 is known to mediate the negative regulation of prepro-TRH gene, its molecular mechanism remains unknown. Our previous studies on the T3-dependent negative regulation of the thyrotropin β subunit (TSHβ) gene indicate the tethering mechanism, where T3-bound TRβ2 interferes with the function of the transcription factor GATA2, which is essential for TSHβ expression. Interestingly, the transcription factor Sim1, a determinant of PVN differentiation in hypothalamus, is reported to induce the expressions of TRβ2 and GATA2. Indeed, our immunohistochemistry revealed the expression of GATA2 in the TRH neuron of the rat PVN. According to the experimental report with transgenic mice, the DNA sequence from nt. -547 to nt. +84 is sufficient for the expression of the prepro-TRH gene in PVN. Using the CAT reporter gene harboring this region, we found that this promoter is activated by GATA2 approximately 6-fold in CV1 cells. The deletion and mutation analyses identified a functional GATA-responsive element (GATA-RE) between nt. -357 and nt. -352. When TRβ2 was co-expressed, T3 reduced GATA2-dependent promoter activity to approximately 30%. T3-dependent repression was maintained after the mutation of the putative negative T3 responsive element (site4). Although the melanocortin 4 receptor signaling is known to stimulate the prepro-TRH promoter via protein kinase A pathway in the PVN, inhibition by T3 was dominant over the 8-bromo-cAMP-induced activation. We observed the in vivo recognition of GATA-RE by GATA2 using chromatin immunoprecipitation assay with CA77 cells, which express endogenous TRH. The electrophoretic mobility shift assay also demonstrated that GATA2 bound to oligonucleotide containing the GATA-RE. These results suggest that, as in the case of the TSHβ gene, GATA2 transactivates the prepro-TRH gene and that T3-bound TRβ2 interferes with its function, resulting in the negative regulation of this gene.

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