Platelet-Rich Fibrin Potentiates Dental Pulp Stem Cell Angiogenesis through Mitochondrial Transfer-Meditated Metabolic-Signaling Integration
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1247407 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33404800_1.fastq.gz | Fastqsanger.gz | |||
| SRR33404800_2.fastq.gz | Fastqsanger.gz | |||
| SRR33404801_1.fastq.gz | Fastqsanger.gz | |||
| SRR33404801_2.fastq.gz | Fastqsanger.gz | |||
| SRR33404802_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Platelet-rich fibrin induces an inflammatory phenotype of U937 macrophages
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Project description:Dental pulp cells (DPCs) are a promising source of transplantable cells in regenerative medicine. However, DPCs have not been fully characterized at the molecular level. The purpose of this study was to distinguish DPCs from various source-derived mesenchymal stem cells, fibroblasts, and other cells by the expression of several DPC-characteristic genes. DPCs were isolated from human pulp tissues by the explant method, or the enzyme digestion method, and maintained with media containing 10% serum or 7.5% platelet-rich plasma. RNA was isolated from the cells and from dental pulp tissue specimens. The mRNA levels were determined by DNA microarray and quantitative real-time PCR analyses. The msh homeobox1 (MSX1), msh homeobox 2 (MSX2), T-box 2 (TBX2), and ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1) mRNA levels in DPCs were higher than the levels found in the following cells: mesenchymal stem cells, derived from bone marrow, synovium, and adipose tissue; and in cells such as fibroblasts, osteoblasts, adipocytes, and chondrocytes. The enhanced expression in DPCs was consistently observed irrespective of donor age, tooth type, and culture medium. Moreover, these genes were expressed at high levels in dental pulp tissue in vivo. We conclude that this gene set may be useful in the identification and characterization of DPCs in basic studies and pulp cell-based regeneration therapy.
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Project description:Transcriptional response of rat dental pulp cells (DPCs) cultured with SAHA at early and late mineralisation time points Transcript profiling of DPC identified several novel genes expression induced and supressed by HDACi at 24 hrs and 14 days under mineralising conditions. SAHA induces several members of the MMP family of endopepsidases (TIMP-1, MMP-9, MMP-13) and other members of the endochondral ossification pathway at 24 h. 8 experiemental parameters were analysed, each carried out in quadruplicate
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Project description:Osteoarthritis (OA) is a degenerative and inflammatory joint disorder with cartilage loss. Dental pulp stem cells (DPSCs) can undergo chondrogenic differentiation and secrete growth factors associated with tissue repair and immunomodulation. Leukocyte- and platelet-rich fibrin (L-PRF) emerges in regenerative medicine because of its growth factor content and fibrin matrix. This study evaluates the therapeutic application of DPSCs and L-PRF in OA via immunomodulation and cartilage regeneration. Chondrogenic differentiation of DPSCs, with or without L-PRF exudate (ex) and conditioned medium (CM), and of bone marrow-mesenchymal stem cells was compared. These cells showed differential chondrogenesis. L-PRF was unable to increase cartilage-associated components. Immature murine articular chondrocytes (iMACs) were cultured with L-PRF ex, L-PRF CM, or DPSC CM. L-PRF CM had pro-survival and proliferative effects on unstimulated and cytokine-stimulated iMACs. L-PRF CM stimulated the release of IL-6 and PGE2, and increased MMP-13, TIMP-1 and IL-6 mRNA levels in cytokine-stimulated iMACs. DPSC CM increased the survival and proliferation of unstimulated iMACs. In cytokine-stimulated iMACs, DPSC CM increased TIMP-1 gene expression, whereas it inhibited nitrite release in 3D culture. We showed promising effects of DPSCs in an in vitro OA model, as they undergo chondrogenesis in vitro, stimulate the survival of chondrocytes and have immunomodulatory effects.
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Project description:Transcriptional response of rat dental pulp cells (DPCs) cultured with SAHA at early and late mineralisation time points Transcript profiling of DPC identified several novel genes expression induced and supressed by HDACi at 24 hrs and 14 days under mineralising conditions. SAHA induces several members of the MMP family of endopepsidases (TIMP-1, MMP-9, MMP-13) and other members of the endochondral ossification pathway at 24 h.
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Project description:Gene expression analysis data of human permanent dental pulp tissues
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Project description:Objectives: Dental pulp stem cells are crucial in immune response regulation. However, sub-clusters of these cells involved in deep caries progression remain unidentified. This study explores the role of Intercellular adhesion molecule 1-positive dental pulp stem cells (ICAM1+DPSCs) within the immune microenvironment of dental pulp tissue affected by deep caries, aiming to establish a theoretical foundation and novel strategies for its prevention and treatment.Methods: Use flow cytometry to sort ICAM1+ DPSCs and ICAM1- DPSCs for RNA-seq.
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