Effect of 5-Aza-2′-deoxycytidine on Odontogenic Differentiation of Human Dental Pulp Cells

Zhang, Deqian; Li, Qimeng; Rao, Lijia; Yi, Benshun; Xu, Qiong

doi:10.1016/j.joen.2014.12.006

Cited by 53 publications

(49 citation statements)

References 32 publications

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“…However, the epigenetic regulatory mechanism underlying miR-200c expression has not been previously studied in human cancer to the best of our knowledge. Aza is a DNA methyltransferase inhibitor, which may cause DNA demethylation (22). In the present study, it was observed that treatment with Aza significantly promoted the expression of miR-200c, in a dose-dependent manner.…”

Section: Discussionsupporting

confidence: 56%

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Demethylation drug 5-Aza-2′-deoxycytidine-induced upregulation of miR-200c inhibits the migration, invasion and epithelial-mesenchymal transition of clear cell renal cell carcinoma in vitro

Jiang

Sun

et al. 2016

Oncology Letters

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Section: Discussionsupporting

confidence: 56%

“…MicroRNAs (miRs) are a type of small non-coding RNA (19)(20)(21)(22)(23)(24)(25) nucleotides) that possess prominent roles in the regulation of genes (6). MiRs typically inhibit gene expression by directly binding the 3'-untranslated region of their target messenger (m)RNAs, causing repression of translation or mRNA degradation (7).…”

Section: Introductionmentioning

confidence: 99%

Demethylation drug 5-Aza-2′-deoxycytidine-induced upregulation of miR-200c inhibits the migration, invasion and epithelial-mesenchymal transition of clear cell renal cell carcinoma in vitro

Jiang

Sun

et al. 2016

Oncology Letters

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“…Elucidating the long‐sought mechanisms that regulate hDPC odontoblastic differentiation would contribute significantly to providing diverse routes in the field of reparative dentinogenesis. Our recent reports implied that DNA methylation/demethylation offers an epigenetic mechanism to illustrate this topic …”

Section: Discussionmentioning

confidence: 99%

“…Our recent reports implied that DNA methylation/demethylation offers an epigenetic mechanism to illustrate this topic. 20,33,35 In 2009, Rao's group first indicated that the TET1 protein can hydroxylate 5mC to 5hmC and initiate the active DNA demethylation pathway. 5 TET1 has been detected subsequently in the foetal heart, brain, adult skeletal muscle and other organs.…”

Section: Discussionmentioning

confidence: 99%

FAM20C could be targeted by TET1 to promote odontoblastic differentiation potential of human dental pulp cells

Feng

et al. 2017

Cell Proliferation

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“…It has been reported that DNA methylation effected reparative dentinogenesis (Zhang et al . ), which also contributes to inflammatory processes by regulating Toll‐like receptor‐2 (TLR2) and TLR4 (Shuto et al . , Takahashi et al …”

Section: Discussionmentioning

confidence: 99%

Inflammation‐induced overexpression of microRNA‐223‐3p regulates odontoblastic differentiation of human dental pulp stem cells by targeting SMAD3

Huang

Liu²,

Hou

et al. 2018

Int Endodontic J

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Aim To profile miRNA expression between inflamed and healthy human dental pulp tissues and to investigate how the upregulation of miR‐223‐3p in the inflamed pulp tissue regulates odontoblast differentiation and regeneration. Methodology Microarray analysis was used to identify differences in miRNA expression patterns between healthy and inflamed pulp tissue. The results were validated using quantitative real‐time PCR. To determine the effect of miR‐223‐3p on odontoblast differentiation, miR‐223‐3p was overexpressed in human dental pulp stem cells (DPSCs), which were cultured in mineralizing induction medium (to induce odontoblast differentiation). To identify the target genes of miR‐223‐3p, an SABiosciences Human Osteogenesis PCR Array, combined with bioinformatics, was used. Furthermore, a dual‐luciferase reporter assay and a small interfering RNA (siRNA) experiment were used to confirm the relationship between miR‐223‐3p and its target gene. Statistical analysis was performed using the Student's t‐test or one‐way analysis of variance (anova); P < 0.05 was considered statistically significant. Results Seventy‐nine miRNAs were significantly differentially expressed (fold change >2.0; P < 0.05) between the two tissues. In particular, miR‐223‐3p was markedly upregulated in inflamed dental pulp. Overexpression of miR‐223‐3p in DPSCs significantly increased the protein levels of dentine sialophosphoprotein (DSPP) and dentine matrix protein 1 (DMP‐1) (P < 0.05). However, the SMAD family member 3 (SMAD3) protein level was significantly lower than in control DPSCs (P < 0.05). Bioinformatics and the dual‐luciferase assay reporter assay indicated that Smad3 was a potential target of miR‐223‐3p. Knockdown of Smad3 in DPSCs subjected to mineralization induction resulted in detection of DSPP and DMP‐1 earlier than in control DPSCs, and it increased the protein level of alkaline phosphatase (ALP), thereby promoting odontoblast differentiation. Conclusions miR‐223‐3p is implicated in the regulation of odontoblast differentiation, which may be involved in the process of pulpitis repair.

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Effect of 5-Aza-2′-deoxycytidine on Odontogenic Differentiation of Human Dental Pulp Cells

Cited by 53 publications

References 32 publications

Demethylation drug 5-Aza-2′-deoxycytidine-induced upregulation of miR-200c inhibits the migration, invasion and epithelial-mesenchymal transition of clear cell renal cell carcinoma in vitro

Demethylation drug 5-Aza-2′-deoxycytidine-induced upregulation of miR-200c inhibits the migration, invasion and epithelial-mesenchymal transition of clear cell renal cell carcinoma in vitro

FAM20C could be targeted by TET1 to promote odontoblastic differentiation potential of human dental pulp cells

Inflammation‐induced overexpression of microRNA‐223‐3p regulates odontoblastic differentiation of human dental pulp stem cells by targeting SMAD3

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