Cellular microenvironment in inflammatory periapical tissue
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA811571 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18208256_1.fastq.gz | Fastqsanger.gz | |||
| SRR18208256_2.fastq.gz | Fastqsanger.gz | |||
| SRR18208257_1.fastq.gz | Fastqsanger.gz | |||
| SRR18208257_2.fastq.gz | Fastqsanger.gz | |||
| SRR18208258_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 17 |
Similar Datasets
Project description:Chronic apical periodontitis, typified by inflammatory granulation tissue formation and alveolar bone destruction, is the immune response around the apical root caused by long-term infection and pathogenic stimulation in the root canal. Through the recruitment and infiltration of immune cells and inflammatory mediators, wound healing begins accompanied by the starting of infection. Hence, a comprehensive understanding of biological processes and disease development from the cellular microenvironment in inflammatory periapical areas has important implications.
2022-03-31 | GSE197680 | GEO
Project description:Control of Inflammatory Response by Tissue Microenvironment
| PRJNA1124074 | ENA
Project description:Control of Inflammatory Response by Tissue Microenvironment [ChIP-Seq]
| PRJNA1124075 | ENA
Project description:Inflammation is an essential defense response but operates at the cost of normal functions. Whether and how the negative impact of inflammation is monitored remains largely unknown. Acidification of the tissue microenvironment is associated with inflammation. Here we investigated whether macrophages sense tissue acidification to adjust inflammatory responses. We found that acidic pH restructured the inflammatory response of macrophages in a gene-specific manner. We identified mammalian BRD4 as a novel intracellular pH sensor. Acidic pH disrupts the transcription condensates containing BRD4 and MED1, via histidine-enriched intrinsically disordered regions. Crucially, decrease in macrophage intracellular pH is necessary and sufficient to regulate transcriptional condensates in vitro and in vivo, acting as negative feedback to regulate the inflammatory response. Collectively, these findings uncovered a pH-dependent switch in transcriptional condensates that enables environmental sensing to directly control inflammation, with a broader implication for calibrating the magnitude and quality of inflammation by the inflammatory cost.
2025-03-20 | GSE269890 | GEO
Project description:Inflammation is an essential defense response but operates at the cost of normal functions. Whether and how the negative impact of inflammation is monitored remains largely unknown. Acidification of the tissue microenvironment is associated with inflammation. Here we investigated whether macrophages sense tissue acidification to adjust inflammatory responses. We found that acidic pH restructured the inflammatory response of macrophages in a gene-specific manner. We identified mammalian BRD4 as a novel intracellular pH sensor. Acidic pH disrupts the transcription condensates containing BRD4 and MED1, via histidine-enriched intrinsically disordered regions. Crucially, decrease in macrophage intracellular pH is necessary and sufficient to regulate transcriptional condensates in vitro and in vivo, acting as negative feedback to regulate the inflammatory response. Collectively, these findings uncovered a pH-dependent switch in transcriptional condensates that enables environmental sensing to directly control inflammation, with a broader implication for calibrating the magnitude and quality of inflammation by the inflammatory cost.
2025-03-20 | GSE269891 | GEO
Project description:We investigated whether the features of donor-derived stromal vascular fraction of perirenal adipose tissue (PRAT-SVF) could be indicative of the deleterious impact of the ECD microenvironment on renal transplants. A comparative analysis of cellular components, transcriptomic and vasculogenic profiles was performed in PRAT-SVF obtained from deceased donors (non ECD) and expanded criteria donors (ECD) The global RNA sequencing approach indicated a differential molecular signature in the PRAT-SVF of ECD donors characterized by the overexpression of inflammatory transcripts (CXCL1, CCL4, IL1-β,INF-ϒ).
2020-04-10 | GSE140122 | GEO
Project description:Pericytes (PCs) are multipotent contractile cells that wrap around the endothelial cells to maintain the blood vessel's functionality and integrity. The hyperglycemia associated with Type 2 diabetes mellitus (T2DM) was shown to impair the function of PCs and increase the risk of diabetes complications. In this study, we aimed to investigate the deleterious effect of the diabetic microenvironment on the regenerative capacities of human PCs. PCs isolated from human adipose tissue were cultured in the presence or absence of serum collected from diabetic patients (DS). The functionality of PCs was analysed after 6, 14, and 30 days. Microscopic examination of PCs cultured in DS (DS-PCs) showed increased aggregate formation and altered surface topography with hyperbolic invaginations. Compared to PCs cultured in normal serum (NS-PCs), DS-PCs showed more fragmented mitochondria and thicker nuclear membrane. DS caused impaired angiogenic differentiation of PCs as confirmed by tube formation, decreased VEGF-A and IGF-1 gene expression, upregulated TSP1, PF4, actin related protein 2/3 complex and downregulated COL21A1 protein expression. These cells suffered higher apoptotis and showed higher expression of Clic4, apoptosis facilitator BCl-2-like protein serine/threonine protein phosphatase, and Caspase-7 proteins. DS-PCs showed dysregulated DNA repair genes CDKN1A, SIRT1, XRCC5 and TERF2 and up-regulation of the pro-inflammatory genes ICAM1, IL-6, and TNF-α. DS treated cells also showed disruption in the expression of the focal adhesion and binding proeins TSP1, TGF- β, fibronectin and PCDH7. DS-PCs showed resistance mechanisms upon exposure to diabetic microenvironment by maitining the intracellular ROS level and upregulation of ECM organizing proteins vinculin, IQGAP1, and tubulin beta chain.These data show that the diabetic microenvironment exert a deleterious effect on the regenerative capacities of human adipose tissue-derived PCs, and may thus have possible implications on the vascular complications of type-2 diabetes mellitus. Nevertheless, their protective mechanisms when initially exposed to DS could provide a promising cellular therapy for T2DM.
2024-05-23 | PXD048187 | Pride
Project description:Non-inflammatory tumor microenvironment of Diffuse Intrinsic Pontine Glioma (DIPG)
| PRJNA474825 | ENA
Project description:Diffuse intrinsic pontine glioma (DIPG) is a universally fatal malignancy of the childhood central nervous system, with a median overall survival of 9-11 months. We have previously shown that primary DIPG tissue contains numerous tumor-associated macrophages, and substantial work has demonstrated a significant pathological role for adult glioma-associated macrophages. However, work over the past decade has highlighted many molecular and genomic differences between pediatric and adult glioblastomas (GBM). Thus, we directly compared inflammatory characteristics of DIPG and adult GBM. We found that the leukocyte (CD45+) compartment in primary DIPG tissue samples is predominantly composed of CD11b+ macrophages, with very few CD3+ T-lymphocytes. In contrast, T-lymphocytes are more abundant in adult GBM tissue samples. RNA sequencing of macrophages isolated from primary tumor samples revealed that DIPG- and adult GBM-associated macrophages both express gene programs related to ECM remodeling and angiogenesis, but DIPG-associated macrophages express substantially fewer inflammatory factors than their adult GBM counterparts. Examining the secretome of glioma cells, we found that patient-derived DIPG cell cultures secrete markedly fewer cytokines and chemokines than patient-derived adult GBM cultures. Concordantly, bulk and single-cell RNA sequencing data indicates low to absent expression of chemokines and cytokines in DIPG. Together, these observations suggest that the inflammatory milieu of the DIPG tumor microenvironment is fundamentally different than adult GBM. The low intrinsic inflammatory signature of DIPG cells may contribute to the lack of lymphocytes and non-inflammatory phenotype of DIPG-associated microglia/macrophages. Understanding the glioma subtype-specific inflammatory milieu may inform the design and application of immunotherapy-based treatments.
2018-08-23 | GSE115397 | GEO
Project description:The role of distinct synovial tissue macrophage populations in shaping synovial tissue microenvironment
| PRJEB37668 | ENA