Cald1 regulates osteogenic differentiation of PDLSCs.
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ABSTRACT:
PROVIDER: PRJNA988422 | ENA |
REPOSITORIES: ENA
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Project description:To explore underlying mechanisim of which Cald1 regulates osteogenic differentiation of PDLSCs, RNA -seq was performed on PDLSCs treated with NC shRNA and Cald1 shRNA respectively.
2025-06-30 | GSE236009 | GEO
Project description:As the primary seed cells in periodontal tissue engineering, the role of periodontal ligament stem cells (PDLSCs) in periodontal tissue regeneration and bone remodeling during orthodontic tooth movement (OTM) has been well documented. Nevertheless, the impact of different polarization states of macrophages on the osteogenic differentiation of PDLSCs is poorly understood. M0, M1 and M2 macrophage-derived exosomes (M0-exo, M1-exo and M2-exo) were treated with primary cultured human PDLSCs, respectively. Identification of differentially expressed microRNAs (DE-miRNA) in M0-exo and M2-exo by miRNA microarray. In summary, we have indicated for the first time that M2-exo can promote osteogenic differentiation of human PDLSCs, and have revealed the functions and pathways involved in the DE-miRNAs of M0-exo and M2-exo and their downstream targets.
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Project description:Ability to perform osteogenic differentiation is one of the minimal criteria of mesenchymal stem cells (MSCs). Still, it is generally unknown whether osteogenic differentiation is universal cell fate or various phenotypically similar cell states. Besides this, MSCs and their secretomes are actively using for cell/cell-free therapy development, but systemic inter-source variation in MSCs secretomes, proteomes and differentiation mechanisms are still poorly understood. Therefore, here we compared proteomic and secretomic profiles of human mesenchymal cells from six sources: osteoblasts (bone), WJ-MSCs (Warton’s jelly), AD-MSCs (adipose), PDLSCs (tooth: Periodontal Ligament Stem Cells), DPSCs (tooth: Dental Pulp Stem Cells) and GFs (tooth: Gingival Fibroblasts). For experiments we used cells in early passages (3-5) isolated from 3-6 individuals. All cells were compared in standard cultivation and in the 10th day after induction of osteogenic differentiation.
2023-11-05 | PXD037320 | Pride
Project description:Periodontal ligament stem cells (PDLSCs) are optimal seed cells for periodontal regeneration; thus, exploration of the mechanisms regulating PDLSCs osteogenic differentiation is critical. Here, tandem mass tag quantitative proteomics and phosphoproteomic analyses of human PDLSCs were carried out after osteogenic differentiation for 14 days. Proteomic analyses identified 314 differentially expressed proteins (DEPs) that were predicted to be mostly extracellular. Gene ontology and pathway enrichment analyses revealed that the mineral absorption signaling pathway was significantly involved. For phosphoproteomics, un-normalized data identified 1016 differentially expressed phosphorylation sites (DEPSs) corresponded to 380 DEPs, whereas in normalized data, 3030 DEPSs were identified, corresponding to 358 DEPs. Overlapping of these data identified 16 phosphorylated DEPs, among which tetratricopeptide repeat protein 17, stanniocalcin-1, and extracellular superoxide dismutase [Cu-Zn] were significantly related. Kyoto
2022-02-25 | PXD031905 |
Project description:Chromodomain helicase DNA-binding protein 7 (CHD7) is an ATP-dependent chromatin remodeling enzyme, functioning as chromatin reader to conduct epigenetic modification. Its effect on osteogenic differentiation of human dental follicle cells (hDFCs) remains unclear. Here we show CHD7 expression increases with osteogenic differentiation. knockdown of CHD7 impairs the osteogenic ability of hDFCs, characterized by reduced alkaline phosphatase activity and mineralization, and decreased expression of osteogenesis-related genes. Conversely, CHD7 overexpression enhances the osteogenic differentiation of hDFCs. Mechanically, RNA-seq analyses revealed the down-regulated enrichment of PTH (parathyroid hormone)/PTH1R (parathyroid hormone receptor-1) signaling pathway after CHD7 knockdown. We found the expression of PTH1R positively correlates with CHD7. Importantly, overexpression of PTH1R in CHD7-knockdown hDFCs partially rescued the impaired osteogenic differentiation. Our research demonstrates that CHD7 regulates the osteogenic differentiation of hDFCs by regulating the transcription of PTH1R.
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Project description:Epigenetics regulates the expression of osteogenic genes and mediates the osteogenic differentiation of MSCs. It was found that hepatoma-derived growth factor (HDGFR2) is a histone methylated reader protein, which can recognize histone methylation modification and play an important "switch" role in gene transcriptional regulation. It is unclear whether HDGFR2 is involved in bone formation studies. Our study aims to investigate the effect of HDGFR2 on osteogenic differentiation and provide evidence for BMSCs as seed cells for tissue regeneration.
2024-04-19 | GSE263961 | GEO
Project description:This study investigated the cellular response of human periodontal ligament stem cells (PDLSCs) to elevated levels of a specific fatty acid (FA), namely, palmitic acid (PA) and the role of long noncoding RNAs (lncRNAs) in regulating PA exposure-compromised osteogenic potential of PDLSCs. It was found that exposure of PDLSCs to abundant PA led to decreased osteogenic differentiation of cells. Through microarray analysis and gain/loss-of-function studies, AC018926.2 was identified and validated as the lncRNA that was most sensitive to PA and a regulator in the process of PDLSC osteogenic differentiation under a PA condition. Then, RNA sequencing and KEGG analysis demonstrated that AC018926.2 upregulated integrin α2 (ITGA2) expression at the transcriptional level and therefore activated ITGA2/FAK/AKT signaling. Further functional studies revealed that inactivation of ITGA2/FAK/AKT signaling by silencing ITGA2 counteracted the enhancement of the PDLSC osteogenic potential induced by AC018926.2 overexpression. Moreover, the results of bioinformatics analysis and the RNA immunoprecipitation (RIP) assay suggested that AC018926.2 might transcriptionally regulate ITGA2 expression by binding to poly (ADP-ribose) polymerase 1 (PARP1). Our data suggest that AC018926.2 plays a crucial role in PA exposure-compromised osteogenic potential of PDLSCs.
2022-11-26 | GSE218434 | GEO
Project description:Treadmill training regulates bone metabolism and osteogenic differentiation(miRNA Array)
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Project description:Epigenetics regulates the expression of osteogenic genes and mediates the osteogenic differentiation of MSCs. It was found that hepatoma-derived growth factor (HDGFR2) is a histone methylated reader protein, which can recognize histone methylation modification and play an important "switch" role in gene transcriptional regulation. It is unclear whether HDGFR2 is involved in bone formation studies. Our study aims to investigate the effect of HDGFR2 on osteogenic differentiation and provide evidence for BMSCs as seed cells for tissue regeneration. We found that compared with the wild-type (WT) mice, the bone mass of the femur and the root furcation bone in HDGFR2-KO mice was significantly elevated to attenuate age-related bone loss. Compared with the BMSCs in WT mice, the cloning and osteogenic differentiation of BMSCs in HDGFR2-KO mice were significantly accelerated, and vice versa when HDGFR2 was overexpressed. GO analysis suggested that differential genes were mainly involved in osteoblast differentiation, ossification, collagen fiber tissue and mineralization. The bone defect repair ability of HDGFR2-KO mice was significantly enhanced compared to the control group. Moreover, the depletion of HDGFR2 suppressed periodontal bone loss. The HDGFR2 interacts with the active regulator of SIRT1 (AROS) and sirtuin family deacetylases to form a chromatin remodeling complex, and AROS regulated osteogenesis through combining with HDFGR2. The decreased ratio of H3K18 crotonylation to acetylation improved the transcription of osteogenic genes in HDGFR2 knockout BMSCs. Taken together, these data demonstrated that the knockdown of HDGFR2 could promote osteogenic differentiation and bone repair, providing a new theoretical basis for bone tissue regeneration.
2024-04-19 | GSE263962 | GEO
Project description:Sexual dimorphism in osteogenic differentiation
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