Genome-wide occupancies of multiple transcription activators in PDLSCs induced by GIPRA
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ABSTRACT:
PROVIDER: PRJEB94126 | ENA |
REPOSITORIES: ENA
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Project description:Our previous study (Environ Pollut. 2023;323:121307) has indicated that Glucose-dependent insulinotropic polypeptide receptor (GIPR) is down-regulated in periodontal ligament stem cells (PDLSCs) by cigarette and E-cig. In the current study, ChIP-seq was conducted to study the genome-wide occupancies of phosphorylated CREB (p-CREB), p-STAT, p-ERK and TCF4 in PDLSCs treated with GIPR agonist (GIPRA) (Pro3) GIP (0.5 nM, 24 h, Cat. No. HY-P3584, MCE, China) and ERK1/2 inhibitor SCH772984 (0.5 μM, 24 h, HY-50846, MCE) compared to normal PDLSCs.
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Project description:Our previous study (Environ Pollut. 2023;323:121307) has indicated that Glucose-dependent insulinotropic polypeptide receptor (GIPR) and Glucagon-like peptide-1 receptor (GLP1R) are down-regulated in periodontal ligament stem cells (PDLSCs) by cigarette and E-cig. In the current study, we focus on investigating the functional roles of these two G protein-coupled receptors in PDLSCs, as well as their molecular mechanisms behind it. In brief, human PDLSCs treated with GIPR-siRNA, GIPR agonist (GIPRA) as well as GIPR, GLP1R dual agonist (2GRA) were used to study the effects of GIPR on cell growth of PDLSCs. Moreover, PDLSCs were induced to undergo osteogenic, adipogenic, chondrogenic, and neurogenic differentiation in vitro. GLP1R siRNA, GLP1R agonist (GLP1RA), and 2GRA were respectively administered to investigate the effects of GLP1R on the differentiation potential of PDLSCs.
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Project description:To study the molecular mechanisms underlying PDLSC osteogenic differentiation, we developed RNA sequencing with Illumina HiSeq2000 to comprehensively identify RNA expression profiles in normal PDLSCs, osteogenic inductive PDLSCs and mechanical force-induced PDLSCs. Plenty of RNAs were found to be differentially expressed by RNA sequencing. Furthermore, the potential functions of these RNAs were investigated using bioinformatic analysis.
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Project description:Cald1 regulates osteogenic differentiation of PDLSCs.
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Project description:Tooth pulp contains various types of cells such as endothelial cells, neurons, fibroblasts, osteoblasts, osteoclasts, and odontoblasts. As well as cells that are called "postnatal dental pulp stem cells" (DPSCs). Also, four more types of dental MSC-like populations were identified and characterized: stem cells from human exfoliated deciduous teeth (SHED), periodontal ligament stem cells (PDLSCs), stem cells from the apical papilla (SCAP) and population of dental follicle-derived progenitor cells called "dental follicle progenitor cells" (DFPCs). Most of them might be used in wide range of biomedical applications. Nevertheless, they have systematic differences in their physiology, e.g. differences in proliferative and differentiation potential. These differences are not clearly defined on molecular level yet; therefore, we performed proteomics comparison of DPSCs and PDLSCs in control and osteogenic differentiation. Donor matched DPSCs and PDLSCs were isolated from two donors by standard protocol. Then, DPSCs and PDLSCs at passage 3 were seeded into 90 mm Petri dishes (Eppendorf) and cultured in standard conditions with DMEM (Gibco) supplemented with 15% fetal bovine serum (FBS), 37°C, 5% CO2. When cells reached 90-100% confluency, the medium was changed to osteogenic medium (DMEM supplemented with 10% FBS, 2 mM L-glutamine, 1% penicillin/streptomycin (HyClone), 50 mg/ml ascorbic acid (Sigma Aldrich), 0.1 mM dexamethasone (Sigma Aldrich) and 10 mM b–glycerophosphate (Sigma Aldrich).
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Project description:RSC (remodels the structure of chromatin) is an essential ATP-dependent chromatin remodeling complex in Saccharomyces cerevisiae. The catalytic subunit of RSC, Sth1 uses its ATPase activity to slide or remove nucleosomes. RSC has been shown to regulate the width of the nucleosome-depleted regions (NDRs) by sliding the flanking nucleosomes away from NDRs. As such the nucleosomes encroach NDRs when RSC is depleted and leads to transcription initiation defects. In this study, we examined the effects of the catalytic-dead Sth1 on transcription and compared them to the effects observed during acute and rapid Sth1 depletion by auxin-induced degron strategy. We found that rapid depletion of Sth1 reduces recruitment of TBP and Pol II in highly transcribed genes, as would be expected considering its role in regulating chromatin structure at promoters. In contrast, cells harboring the catalytic-dead Sth1 exhibited a severe reduction in TBP binding, but surprisingly, also displayed a substantial accumulation in Pol II occupancies within coding regions. After depleting endogenous Sth1 in the catalytic dead mutant, we observed a further increase in Pol II occupancies, suggesting that the inactive Sth1 contributed to the observed accumulation of Pol II in coding regions. Notwithstanding the Pol II increase, the ORF occupancies of histone chaperones FACT and Spt6 were significantly reduced in the mutant. These results suggest a potential role for RSC in recruiting/retaining these chaperones in coding regions. Pol II accumulation despite substantial reductions in TBP, FACT, and Spt6 occupancies in the catalytic-dead mutant could be indicative of severe transcription elongation and termination defects. Such defects would be consistent with studies showing that RSC is recruited to coding regions in a transcription-dependent manner. Thus, these findings imply a role for RSC in transcription elongation and termination processes, in addition to its established role in transcription initiation.
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