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Project description:Chromatin accessibility is key epigenomic regulatory mechanisms of transcription. Herein, to profile open chromatin maps and transcriptional feature associated with odontogenic tropism of dental pulp stem cells (DPSCs), we conducted integrative analysis of epigenomic alteration and transcriptome changes during odontogenic differentiation of DPSCs. DPSCs were long-term cultured in odontogenic induction medium to evaluate differentiation abilities. ATAC-seq and RNA-seq samples were collected before and after the 9-day culture. One of the day 9 specific-super-enhancer was constructed in ALPL (Alkaline Phosphatase, Biomineralization Associated) intragenic region in which all the day 9-specific open chromatin peaks were included and BMP-mediated Smad binding element are specifically accumulated. These results suggest that the specific local chromatin regions were selectively opened and, particularly, super-enhancers were constructed, which was able to guide differentiative transcriptional factors such as Smad1/4 to their target gene loci in differentiating DPSCs; hence, epigenetic modifications such as histone deacetylase (HDACs) inhibitor application have therapeutic potential for DPSCs-induced dentin/pulp regeneration.
2023-09-29 | GSE244058 | GEO
Project description:Chromatin accessibility is key epigenomic regulatory mechanisms of transcription. Herein, to profile open chromatin maps and transcriptional feature associated with odontogenic tropism of dental pulp stem cells (DPSCs), we conducted integrative analysis of epigenomic alteration and transcriptome changes during odontogenic differentiation of DPSCs. DPSCs were long-term cultured in odontogenic induction medium to evaluate differentiation abilities. ATAC-seq and RNA-seq samples were collected before and after the 9-day culture. One of the day 9 specific-super-enhancer was constructed in ALPL (Alkaline Phosphatase, Biomineralization Associated) intragenic region in which all the day 9-specific open chromatin peaks were included and BMP-mediated Smad binding element are specifically accumulated. These results suggest that the specific local chromatin regions were selectively opened and, particularly, super-enhancers were constructed, which was able to guide differentiative transcriptional factors such as Smad1/4 to their target gene loci in differentiating DPSCs; hence, epigenetic modifications such as histone deacetylase (HDACs) inhibitor application have therapeutic potential for DPSCs-induced dentin/pulp regeneration.
2023-09-29 | GSE244057 | GEO
Project description:Integrative epigenomic and transcriptomic anlaysis of odontogenic differentiation of dental pulp stem cells
| PRJNA1021169 | ENA
Project description:Integrative epigenomic and transcriptomic anlaysis of odontogenic differentiation of dental pulp stem cells [RNA-seq]
| PRJNA1021174 | ENA
Project description:Integrative epigenomic and transcriptomic anlaysis of odontogenic differentiation of dental pulp stem cells [ATAC-seq]
| PRJNA1021175 | ENA
Project description:Dental pulp stem cells (DPSCs) have great potential for use in tissue engineering (TE)-based dental treatments. Electrical stimulation (EStim) has been shown to influence cellular functions that could play an important role in the success of TE treatments. Despite many recent studies focused on DPSCs, few have investigated the effect EStim has on these cells. The aim of this research was to investigate the effects of direct current (DC) EStim on osteo-/odontogenic differentiation of DPSCs. To do so cells were isolated from male Sprague Dawley rats (7-8 weeks old), and phenotype characterization and multilineage differentiation analysis were conducted to verify their "stemness." Different voltages of DC EStim were administrated 1 h/day for 7 days, and the effect of EStim on DPSC osteo-/odontogenic differentiation was assessed by measuring calcium and collagen deposition, alkaline phosphatase (ALP) activity, and expression of osteo- and odontogenic marker genes at days 7 and 14 of culture. We found that while 10 and 50 mV/mm of EStim had no effect on cell number or metabolic activity, 100 mV/mm caused a significant reduction in cell number, and 150 mV/mm resulted in cell death. Despite increased gene expression of osteo-/odontogenic gene markers, Osteocalcin, RunX2, BSP, and DMP1, at day 7 in EStim treated cells, 50 mV/mm of EStim decreased collagen deposition and ALP activity at both time points, and calcium deposition was found to be lower at day 14. In conclusion, under the conditions tested, EStim appears to impair DPSC osteo-/odontogenic differentiation. Additional studies are needed to further characterize and understand the mechanisms involved in DPSC response to EStim, with an eye toward its potential use in TE-based dental treatments.
| S-EPMC7337168 | biostudies-literature
Project description:In addition to bone, the dentin-pulp complex is also influenced by menopause, showing a decreased regenerative capacity. High levels of follicle-stimulating hormone (FSH) during menopause could directly regulate bone metabolism. Here, the role of FSH in the odontogenic differentiation of the dentin-pulp complex was investigated. Dental pulp stem cells (DPSCs) were isolated. CCK-8 assays, cell apoptosis assays, Western blotting (WB), real-time RT-PCR, alkaline phosphatase activity assays, and Alizarin Red S staining were used to clarify the effects of FSH on the proliferation, apoptosis and odontogenic differentiation of the DPSCs. MAPK pathway-related factors were explored by WB assays. FSH and its inhibitor were used in OVX rats combined with a direct pulp-capping model. HE and immunohistochemistry were used to detect reparative dentin formation and related features. The results indicated that FSH significantly decreased the odontogenic differentiation of the DPSCs without affecting cell proliferation and apoptosis. Moreover, FSH significantly activated the JNK signalling pathway, and JNK inhibitor partly rescued the inhibitory effect of FSH on DPSC differentiation. In vivo, FSH treatment attenuated the dentin bridge formation and mineralization-related protein expression in the OVX rats. Our findings indicated that FSH reduced the odontogenic capacity of the DPSCs and was involved in reparative dentinogenesis during menopause.
| S-EPMC7521281 | biostudies-literature
Project description:IntroductionOdontogenic differentiation of human dental pulp stem cells (hDPSCs) is a key step of pulp regeneration. Recent studies showed that circular RNAs (circRNAs) have many biological functions and that competing endogenous RNA (ceRNA) is their most common mechanism of action. However, the role of circRNAs in hDPSCs during odontogenesis is still unclear.MethodsIsolated hDPSCs were cultured in essential and odontogenic medium. Total RNA was extracted after 14 days of culture, and then, microarray analysis was performed to measure the differential expressions of circRNAs. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was then performed to validate the microarray results. Based on microarray data from this study and available in the database, a ceRNA network was constructed to investigate the potential function of circRNAs during odontogenesis. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to investigate the potential correlation between signaling pathways and circRNAs. In addition, qRT-PCR and Western blot analysis were used to explore the function of hsa_circRNA_104101.ResultsWe found 43 upregulated circRNAs and 144 downregulated circRNAs during the odontogenic differentiation process (fold change > 1.5 and <-1.5, respectively; P < 0.05). qRT-PCR results were in agreement with the microarray results. Bioinformatic analysis revealed that the Wnt signaling pathway and the TGF-β signaling pathway, as well as the other pathways associated with odontogenic differentiation, were correlated to the differentially expressed circRNAs. hsa_circRNA_104101 was proved to promote the odontogenic differentiation of hDPSCs.ConclusionThis study reported 187 circRNAs that were differentially expressed in hDPSCs during odontogenic differentiation. Bioinformatic analysis of the expression data suggested that circRNA-miRNA-mRNA networks might act as a crucial mechanism for hDPSC odontogenic differentiation, providing a theoretical foundation for the study of pulp regeneration regulation by circRNAs.
| S-EPMC7482017 | biostudies-literature
Project description:Retinoic acid (RA) signal is involved in tooth development and osteogenic differentiation of mesenchymal stem cells (MSCs). Dental pulp stem cells (DPSCs) are one of the useful MSCs in tissue regeneration. However, the function of RA in osteo/odontogenic differentiation of DPSCs remains unclear. Here, we investigated the expression pattern of RA in miniature pig tooth germ and intervened in the RA signal during osteo/odontogenic differentiation of human DPSCs. Deciduous canine (DC) germs of miniature pigs were observed morphologically, and the expression patterns of RA were studied by in situ hybridization (ISH). Human DPSCs were isolated and cultured in osteogenic induction medium with or without RA or BMS 493, an inverse agonist of the pan-retinoic acid receptors (pan-RARs). Alkaline phosphatase (ALP) activity assays, alizarin red staining, quantitative calcium analysis, CCK8 assay, osteogenesis-related gene expression, and in vivo transplantation were conducted to determine the osteo/odontogenic differentiation potential and proliferation potential of DPSCs. We found that the expression of RAR? and CRABP2 decreased during crown calcification of DCs of miniature pigs. Activation of RA signal in vitro inhibited ALP activities and mineralization of human DPSCs and decreased the mRNA expression of ALP, osteocalcin, osteopontin, and a transcription factor, osterix. With BMS 493 treatment, the results were opposite. Interference in RA signal decreased the proliferation of DPSCs. In vivo transplantation experiments suggested that osteo/odontogenic differentiation potential of DPSCs was enhanced by inversing RA signal. Our results demonstrated that downregulation of RA signal promoted osteo/odontogenic differentiation of DPSCs and indicated a potential target pathway to improve tissue regeneration.
| S-EPMC7336240 | biostudies-literature
Project description:Nitric oxide (NO) is thought to play a pivotal regulatory role in dental pulp tissues under both physiological and pathological conditions. However, little is known about the NO functions in dental pulp stem cells (DPSCs). We examined the direct actions of a spontaneous NO gas-releasing donor, NOC-18, on the odontogenic capacity of rat DPSCs (rDPSCs). In the presence of NOC-18, rDPSCs were transformed into odontoblast-like cells with long cytoplasmic processes and a polarized nucleus. NOC-18 treatment increased alkaline phosphatase activity and enhanced dentin-like mineralized tissue formation and the expression levels of several odontoblast-specific genes, such as runt related factor 2, dentin matrix protein 1 and dentin sialophosphoprotein, in rDPSCs. In contrast, carboxy-PTIO, a NO scavenger, completely suppressed the odontogenic capacity of rDPSCs. This NO-promoted odontogenic differentiation was activated by tumor necrosis factor-NF-κB axis in rDPSCs. Further in vivo study demonstrated that NOC-18-application in a tooth cavity accelerated tertiary dentin formation, which was associated with early nitrotyrosine expression in the dental pulp tissues beneath the cavity. Taken together, the present findings indicate that exogenous NO directly induces the odontogenic capacity of rDPSCs, suggesting that NO donors might offer a novel host DPSC-targeting alternative to current pulp capping agents in endodontics.
| S-EPMC5821879 | biostudies-literature