RNAseq of peripheral blood mononucleated cells exposed to platelet-rich fibrin and enamel matrix derivatives.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1109308 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28963220.fastq.gz | Fastqsanger.gz | |||
| SRR28963221.fastq.gz | Fastqsanger.gz | |||
| SRR28963222.fastq.gz | Fastqsanger.gz | |||
| SRR28963223.fastq.gz | Fastqsanger.gz | |||
| SRR28963224.fastq.gz | Fastqsanger.gz |
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Project description:Platelet-rich fibrin (PRF) and Enamel Matrix Derivatives (EMD) can support the local regenerative events in periodontal defects. There is reason to suggest that PRF and EMD exert part of their activity by targeting the blood-derived cells accumulating in the early wound healing blastema. However, the impact of PRF and EMD on blood cell response remains to be discovered. To this aim, we have exposed human peripheral blood mononucleated cells (PBMCs) to PRF lysates and EMD, followed by bulk RNA sequencing. A total of 111 and 8 genes are up- and down-regulated by PRF under the premise of an at least log2 two-fold change and a minus log10 significance level of two, respectively. Representative is a characteristic IFN response indicated by various human leukocyte antigens (HLA-DPA1, HLA-DPB1, HLA-DQA1, HLA-DQA2, HLA-DRA, HLA-DRB1, HLA-DRB5), gamma Fc receptors (FCGR1A, FCGR1B, FCGR3B), chemokines (CXCL9-11), and calprotectin (S100A8/9 and S100A12), complement (C1QA/B, C2) and interferon-induced guanylate-binding proteins (GBP1, GBP5). With EMD, 67 and 29 genes are up- and down-regulated, respectively. Characteristics of the upregulated genes are tensins (TNS1 and TNS3). Among the genes downregulated by EMD were epsilon Fc receptors (FCER1A; FCER2) and Fc receptor-like proteins (FCRL1, FCRL3) and CX3CR1. Genes commonly upregulated by PRF and EMD were most noticeably NXPH4 and MN1, but also FN1, MMP14, MERTK, and AXL. Our findings suggest that PRF provokes an inflammatory response, while EMD dampens IgE signaling in peripheral mononucleated blood cells.
2025-02-05 | GSE266995 | GEO
Project description:RNAseq of peripheral blood mononucleated cells exposed to platelet-rich fibrin and enamel matrix derivatives
| PRJEB75324 | ENA
Project description:Therapeutic angiogenesis in inflammatory microenvironments is constrained by mitochondrial dysfunction in mesenchymal stem cells (MSCs). This study demonstrates that platelet-rich fibrin (PRF) serves as a mitochondrial reservoir that transfers functional mitochondria to dental pulp stem cells (DPSCs) via extracellular vesicle-dependent mechanisms. Multi-omics analyses revealed that PRF-derived mitochondria activated the tricarboxylic acid (TCA) cycle in DPSCs, driving concurrent fatty acid biosynthesis and JAK2/STAT4-mTOR pathway activation. This metabolic-signaling integration enhanced VEGF secretion and cell migration under inflammatory conditions. PRF’s fibrin matrix further sustained mitochondrial release while providing topological guidance for DPSC recruitment. In vivo, PRF-DPSC composites significantly accelerated wound closure and neovascularization compared to controls, supported by histomorphometric and molecular analyses. Beyond cytokine delivery, this work establishes PRF as a mitochondrial-augmented biomaterial to reverse MSC metabolic insufficiency, offering a translatable strategy for vascular regeneration in hostile microenvironments.
2025-04-10 | GSE293909 | GEO
Project description:Platelet-rich fibrin (PRF) is widely used to support local healing, a process that requires the transient polarization of macrophages towards an inflammatory phenotype. PRF and blood clot components, in general, can potentially incite this macrophage response. To test this hypothesis, we performed a screening assay to identify the overall response of macrophages to PRF. To this aim, U937, a histiocytic lymphoma cell line, and THP1, a leukemia cell line, both commonly used bioassays to study macrophage responses, were exposed to PRF lysates. Transcriptomic changes were identified by bulk RNA sequencing. Analysis was based on significantly regulated genes with an adjusted p-value of p<0.05. In U937 macrophages, consistent with our hypothesis, the clustering of increased genes revealed chemokine activity (CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, FCGR3A), prostaglandin biosynthetic process (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, PTGS1) and collagen catabolic process (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19 and MRC2). In THP1 cells, clustering highlighted only steroid biosynthesis. These findings emphasize U937 as an appropriate bioassay to study inflammatory macrophage polarization upon PRF exposure, being consistent with clinical macrophage signatures during early wound healing and holding the potential to recover inflammatory macrophages in chronic wounds.
2025-09-21 | GSE308204 | GEO
Project description:Platelet-rich fibrin (PRF) and Enamel Matrix Derivatives (EMD) can support the local regenerative events in periodontal defects. There is reason to suggest that PRF and EMD exert part of their activity by targeting the blood-derived cells accumulating in the early wound healing blastema. However, the impact of PRF and EMD on blood cell response remains to be discovered. To this aim, we have exposed human peripheral blood mononucleated cells (PBMCs) to PRF lysates prepared by a swing-out rotor and EMD, followed by bulk RNA sequencing. A total of 111 and 8 genes are up- and down-regulated by PRF under the premise of an at least log2 two-fold change and a minus log10 significance level of two, respectively. Representative is a characteristic IFN response indicated by various human leukocyte antigens (HLA-DPA1, HLA-DPB1, HLA-DQA1, HLA-DQA2, HLA-DRA, HLA-DRB1, HLA-DRB5), gamma Fc receptors (FCGR1A, FCGR1B, FCGR3B), chemokines (CXCL9-11), and calprotectin (S100A8/9 and S100A12), complement (C1QA/B, C2) and interferon-induced guanylate-binding proteins (GBP1, GBP5). With EMD, 67 and 29 genes are up- and down-regulated, respectively. Characteristic of the upregulated genes are tensins (TNS1 and TNS3). Among the genes downregulated by EMD were epsilon Fc receptors (FCER1A; FCER2), Fc receptor-like proteins (FCRL1, FCRL3) and CX3CR1. Genes commonly upregulated by PRF and EMD were most noticeably NXPH4 and MN1, as well as FN1, MMP14, MERTK, and AXL. Our findings suggest that PRF provokes an inflammatory response, while EMD dampens IgE signaling in peripheral mononucleated blood cells.
| S-EPMC11779933 | biostudies-literature
Project description:Leukocyte-platelet rich fibrin (L-PRF) is extensively used in the dentistry field and other clinical scenarios due to its regeneration properties. We obtained L-PRF membranes in absence of anticoagulants and cultured in DMEM. The secretomewas collected at days 3, 7 and 21 in order to identify the proteins secreted and the differences over time. Protein secretomeat day 3 was analysed by LC-MS/MS and differences in the proteome were analysed by Sequential Window Acquisition of all Theoretical Mass Spectra (SWATH). Overall, 705 proteins were identified in the secretome of L-PRF membranes after 3 days of culture, including growth factors (EGF, PDGFA) and proteins related to platelet and neutrophil degranulation. A total of 202 differentially secreted proteins were quantified by SWATH when comparing secretomes at days 3, 7 and 21. The majority of them were enriched at day 3 such as MMP9, TSP1 and CO3. On the contrary, fibrinogen and CATS were found down-regulated at day 3. Growth factor and western blotting analysis corroborated the proteomic results. This is the most detailed proteome analysis of the L-PRF secretome to date. Proteins and growth factors identified, and their kinetics, provide novel information to further understand the wound healing properties of L-PRF.
2021-09-09 | PXD017963 | Pride
Project description:Platelet-Rich Fibrin Potentiates Dental Pulp Stem Cell Angiogenesis through Mitochondrial Transfer-Meditated Metabolic-Signaling Integration
| PRJNA1247407 | ENA
Project description:Collagen- and fibrin-based gels are extensively used to study cell behaviour. However, 2D-3D, collagen-fibrin, and in vivo-in vitro comparisons of gene expression, cell shape and mechanotransduction have not been reported. Here we compared chick tendon fibroblasts (CTFs) at three stages of embryonic development with CTFs cultured in collagen- or fibrin-based tissue engineered constructs (TECs).
2015-09-30 | E-MTAB-3488 | biostudies-arrayexpress
Project description:BackgroundPlatelet-rich fibrin (PRF) membranes can preserve alveolar ridge dimension after tooth extraction. Thus, it can be presumed that PRF suppresses the catabolic events that are caused by osteoclastic bone resorption.MethodsTo address this possibility, we investigated the impact of soluble extracts of PRF membranes on in vitro osteoclastogenesis in murine bone marrow cultures. Osteoclastogenesis was induced by exposing murine bone marrow cultures to receptor activator of nuclear factor kappa B ligand (RANKL), macrophage colony-stimulating factor (M-CSF) and transforming growth factor-beta 1 (TGF-β1) in the presence or absence of PRF. Osteoclastogenesis was evaluated based on histochemical, gene expression, and resorption analysis. Viability was confirmed by formation of formazan crystals, live-dead staining and caspase-3 activity assay.ResultsWe report here that in vitro osteoclastogenesis is greatly suppressed by soluble extracts of PRF membranes as indicated by tartrate-resistant acid phosphatase (TRAP) staining and pit formation. In support of the histochemical observations, soluble extracts of PRF membranes decreased expression levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cell-specific transmembrane protein (DCSTAMP), nuclear factor of activated T-cells (NFATc1), and osteoclast-associated receptor (OSCAR). PRF membranes, however, cannot reverse the process once osteoclastogenesis has evolved.ConclusionThese in vitro findings indicate that PRF membranes can inhibit the formation of osteoclasts from hematopoietic progenitors in bone marrow cultures. Overall, our results imply that the favorable effects of PRF membranes in alveolar ridge preservation may be attributed, at least in part, by the inhibition of osteoclastogenesis.
| S-EPMC7155126 | biostudies-literature
Project description:DLX3 is a homeodomain transcription factor involved in ameloblast differentiation and enamel formation. Mutations in DLX3 in human lead to defects in enamel. However, the downstream targets of Dlx3 transcriptional activity in the enamel organ have not been identified yet. In this study, we compared the transcriptome of enamel organs where Dlx3 has been deleted to control tissues. Total RNA was extracted from enamel organs (mandibular incisors) from Dlx3-WT (N=4) and Dlx3-K14cKO (N=4) mice at P10. cDNA libraries were generated using NEBnext and NuGen kits. Sequencing was performed on the HiSeq2000.
2015-05-14 | E-GEOD-57984 | biostudies-arrayexpress