Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243056 | ENA |
REPOSITORIES: ENA
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Project description:In addition to satisfying the metabolic demands of cells, mitochondrial metabolism helps regulate immune cell function. To date, such cell-intrinsic metabolic-immunologic cross-talk has only been described operating in cells of the immune system. Here we show that epidermal cells utilize fatty acid β-oxidation to fuel their contribution to the immune response during cutaneous inflammation. By live imaging metabolic and immunological processes within intact zebrafish embryos during cutaneous inflammation, we uncover a mechanism where elevated β-oxidation-fueled mitochondria-derived reactive oxygen species within epidermal cells helps guide matrix metalloproteinase-driven leukocyte recruitment. This mechanism requires the activity of a zebrafish homolog of the mammalian mitochondrial enzyme, Immunoresponsive gene 1. This study describes the first example of metabolic reprogramming operating within a non-immune cell type to help control its contribution to the immune response. Targeting of this metabolic-immunologic interface within keratinocytes may prove useful in treating inflammatory dermatoses. In this study, Affymetrix Zebrafish Genome Arrays were used to identify zebrafish Irg1l (a homolog of mammalian IRG1) as a gene up-regulated in response to Salmonella infection. The microarray analysis compared 4 day post fertilisation (dpf) dissected larval zebrafish trunks (approximately 50) that had been injected at 2 dpf with either: (i) PBS (as a negative control) or (ii) live Salmonella enterica serovar Typhimurium bacteria. The study was performed in triplicate.
2014-04-01 | E-GEOD-56365 | biostudies-arrayexpress
Project description:In addition to satisfying the metabolic demands of cells, mitochondrial metabolism helps regulate immune cell function. To date, such cell-intrinsic metabolic-immunologic cross-talk has only been described operating in cells of the immune system. Here we show that epidermal cells utilize fatty acid β-oxidation to fuel their contribution to the immune response during cutaneous inflammation. By live imaging metabolic and immunological processes within intact zebrafish embryos during cutaneous inflammation, we uncover a mechanism where elevated β-oxidation-fueled mitochondria-derived reactive oxygen species within epidermal cells helps guide matrix metalloproteinase-driven leukocyte recruitment. This mechanism requires the activity of a zebrafish homolog of the mammalian mitochondrial enzyme, Immunoresponsive gene 1. This study describes the first example of metabolic reprogramming operating within a non-immune cell type to help control its contribution to the immune response. Targeting of this metabolic-immunologic interface within keratinocytes may prove useful in treating inflammatory dermatoses. In this study, Affymetrix Zebrafish Genome Arrays were used to identify zebrafish Irg1l (a homolog of mammalian IRG1) as a gene up-regulated in response to Salmonella infection.
2014-04-01 | GSE56365 | GEO
Project description:Matrix metalloproteinase-9 in chronic lymphocytic leukemia
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Project description:Distinct roles for matrix metalloproteinases 2 and 9 in hematopoietic stem cell emergence, migration and niche colonization
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Project description:Peripheral immune-derived matrix metalloproteinase promotes stress susceptibility
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Project description:Macrophages orchestrate tissue remodeling, inflammation, and metabolic dysfunction in obesity, yet how macrophage-intrinsic extracellular proteolysis integrates with immunometabolic reprogramming remains poorly defined. Matrix metalloproteinase-14 (MMP14), a membrane-anchored protease with broad matrix-remodeling capacity, is markedly induced during monocyte-to-macrophage differentiation and further upregulated in adipose tissue macrophages from high-fat diet (HFD)-fed mice. Pharmacologic inhibition or myeloid-specific deletion of Mmp14 impaired macrophage differentiation, proliferation, migration, and phagocytosis, and blunted pro-inflammatory activation in response to obese adipose tissue–derived cues. Mechanistically, MMP14 enhanced inflammatory programming in part by promoting endotrophin generation and amplifying TLR4-NF-κB signaling. In parallel, MMP14 reshaped macrophage lipid metabolism by suppressing lipolysis and fostering lipid accumulation, thereby modifying macrophage-derived metabolic signals to neighboring cells. In vivo, myeloid-specific Mmp14 deletion protected mice from HFD-induced insulin resistance, dyslipidemia, hepatic steatosis, and adipose tissue inflammation and fibrosis, while increasing energy expenditure and fatty acid utilization. Collectively, these findings identify macrophage MMP14 as a central node linking extracellular matrix remodeling to inflammatory and metabolic dysfunction in obesity.
2026-06-22 | GSE335244 | GEO
Project description:Epidermal function is maintained through a continuous process called epidermal homeostasis, in which keratinocytes gradually differentiate from proliferating stem cells to dead corneocytes that shed off the skin. We investigated the metabolic rewiring that occur during keratinocyte differentiation. We analyzed endometabolome, exometabolome and transcriptome during differentiating in vitro under high calcium conditions. Using network-based computational approaches, we found that proliferating keratinocytes gain energy through branched-chain amino acid-fueled TCA cycle that is shut down during differentiation. Upon differentiation, metabolism is repurposed to serve two main purposes. First, to form the epidermal barrier. Specifically, glucose and nucleotides are utilized for the formation of the lipid-enriched hydrophobic extracellular matrix, the transformation from keratinocytes to corneocytes and their cross-linking. Second, we found active regulation of metabolites with signaling functions during differentiation including hydrocortisone, sphingosines, and exonucleotides. Functional relevance of these findings was tested experimentally by 14 metabolic perturbations that were inferred by our analysis, and effectively affected keratinocytes differentiation and proliferation. Overall, this work provides an integrated and mechanistic analysis of the metabolic underpinnings that sustain epidermal function.
2020-01-01 | GSE136375 | GEO
Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by hair follicle stem cells (HFSCs). We used RNA-seq to identify SOX9-dependent transcriptional changes and ChIP-seq to identify SOX9-bound genes in HF-SCs. Telogen quiescent hair follicle stem cells (HFSCs) and intefollicular epidermal cells (IFE) were FACS-purified for ChIP-sequcencing and HFSCs for RNA-Sequencing
2014-01-28 | E-GEOD-54424 | biostudies-arrayexpress
Project description:Tumors and tumor surrounding tissues produce multiple growth factors that influence tumor cell behavior via different signal transduction pathways. Growth factors like transforming growth factor beta (TGFβ) and epidermal growth factor (EGF) were shown to induce proliferation, migration and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of TGFβ, EGF and the combination of both factors on A549 cells. Both factors stimulated A549 migration to a similar extent but with a different kinetic and the combination had an additive effect. While EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway, this pathway was dispensable for TGFβ-induced migration despite a strong activation by TGFβ. Proteome analysis revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF but only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, EGF was unable to increase invasion of A549 cells on its own and failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF may partly compensate each other for stimulation of cell migration but abrogation of TGFβ signaling may be more suitable for antagonizing invasion.
2021-04-08 | PXD023024 | Pride
Project description:ID1 and CEBPA coordinate epidermal progenitor cell
| PRJNA888130 | ENA