Ontology highlight
ABSTRACT:
PROVIDER: PRJNA860279 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20324215_1.fastq.gz | Fastqsanger.gz | |||
| SRR20324215_2.fastq.gz | Fastqsanger.gz | |||
| SRR20324216_1.fastq.gz | Fastqsanger.gz | |||
| SRR20324216_2.fastq.gz | Fastqsanger.gz | |||
| SRR20324217_1.fastq.gz | Fastqsanger.gz |
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Project description:Studies have shown that the small molecular compound kinsenoside (KD) can inhibit the M1 polarization of macrophages and inhibit the expression of proinflammatory genes. However, the role of kinsenoside in acute pancreatitis is unclear. Our study showed that intraperitoneal injection of kinsenoside can alleviate acute pancreatitis in mice. In order to find out the main mechanism by which kinsenoside affects the polarization of macrophages in acute pancreatitis, we further performed transcriptomic analysis of bone marrow-derived macrophages (BMDMs) stimulated by injured pancreatic acinar cell conditioned media (PAC-CM) treated with or without kinsenoside. This work provides a potential therapeutic approach for acute pancreatitis.
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Project description:Cell death frequently occurs in the pathogenesis of obesity and non-alcoholic fatty liver disease (NAFLD). However, the exact contribution of core cell death machinery to disease manifestations remains ill defined. Here, we show via the direct comparison of mice genetically deficient in apoptotic caspase-8 in myeloid cells, or the essential necroptotic regulators, Receptor-interacting protein kinase-3 (RIPK3) and Mixed lineage kinase domain-like (MLKL), that RIPK3-caspase-8 signaling regulates macrophage inflammatory responses and drives adipose tissue inflammation and NAFLD upon high-fat diet feeding. In contrast, MLKL, divergent to RIPK3, contributes to both obesity and NAFLD in a manner largely independent of inflammation. We also uncover that MLKL regulates the expression of molecules involved in lipid uptake, transport and metabolism and, congruent with this, we discover a shift in the hepatic lipidome upon MLKL deletion. Collectively, these findings highlight MLKL as an attractive therapeutic target to combat the growing obesity pandemic and metabolic disease.
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Project description:This two-color miRNA chip was perfored to identify the downstream miRNAs regulated by Notch signaling in macrophage polarization. To identify the downstream miRNAs mediated by Notch signaling during macrophage polarization regulating, RNA was isolated from bone marrow drived macrophages (BMDMs) of Notch signaling deletion and wild type mice as experiment samples. Three control (+/-) and three experiment (-/-) samples were detected.
2015-03-28 | E-GEOD-67364 | biostudies-arrayexpress
Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, M-NM-14M-NM-21 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis. Bone marrow derived macrophages from five wild type and five Rac2 -/- mutant C57BL mice.
2012-10-02 | E-GEOD-41236 | biostudies-arrayexpress
Project description:Acute pancreatitis (AP) is a common and severe inflammatory disease of the abdomen. Recent studies have shown that macrophages play a crucial role in AP. 4-octyl itaconate (4OI), a derivative of the cell metabolism intermediate itaconate (ITA), has demonstrated significant anti-inflammatory effects in various cell and disease models. In this study, we investigated the potential role and mechanism of 4OI in both in vivo and in vitro models of AP.After administering 25 mg/kg of 4OI to mice and inducing AP with caerulein or L-Arg, we found that 4OI significantly alleviated the severity of AP: serum amylase and lipase levels were significantly reduced, histopathological scores decreased, and levels of inflammatory factors were notably lower. Additionally, macrophage infiltration and M1 polarization were significantly reduced. Through in vitro experiments, we further explored the molecular mechanism by which 4OI inhibits the inflammatory response in macrophages. We discovered that 4OI reduces macrophage polarization to the pro-inflammatory M1 type and decreases the expression of inflammation-related genes. We also found that 4OI exerts its anti-inflammatory effects by promoting the Nrf2 signaling pathway and inhibiting the Sting signaling pathway. In conclusion, this study reveals the anti-inflammatory effects of 4OI in AP and its potential clinical therapeutic value.
2024-09-18 | GSE277097 | GEO
Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, α4β1 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis. SmoA1 Tg MB tumor cells were sorted into CD15+ and CD15- populations. RNA from these samples were hybridized to Affymetrix Mouse Genome 1.0 ST array.
2012-11-15 | E-GEOD-41717 | biostudies-arrayexpress
Project description:BACKGROUND & AIMS: Acinar cells produce digestive enzymes that impede transcriptomic characterization of the exocrine pancreas. Thus, single-cell RNA-sequencing (scRNA-seq) studies of the pancreas underrepresent acinar cells relative to histological expectations, and a robust approach to capture pancreatic cell responses in disease states is needed. We sought to innovate a method that overcomes these challenges to accelerate study of the pancreas in health and disease. METHODS: We introduce FixNCut, a scRNA-seq approach where tissue is reversibly fixed with dithiobis(succinimidyl propionate) prior to dissociation and single-cell preparation. We apply FixNCut to an established mouse model of acute pancreatitis, validate findings using GeoMx whole transcriptome atlas (WTA) profiling, and integrate our data with prior studies to benchmark our method in both mouse and human pancreas datasets. RESULTS: FixNCut achieves unprecedented definition of challenging pancreatic cells including acinar and immune populations in homeostasis and acute pancreatitis, and identifies changes in all major cell types during injury and recovery. We define the acinar transcriptome during homeostasis and acinar-to-ductal metaplasia and establish a unique gene set to measure deviation from normal acinar identity. We characterize pancreatic immune cells, and analysis of T-cell subsets reveals a polarization of the homeostatic pancreas towards type-2 immunity. We report immune responses during acute pancreatitis and recovery, including early neutrophil infiltration, expansion of dendritic cell subsets, and a substantial shift in the transcriptome of macrophages due to both resident macrophage activation and monocyte infiltration. CONCLUSIONS: FixNCut preserves pancreatic transcriptomes to uncover novel cell states during homeostasis and following pancreatitis, establishing a broadly applicable approach and reference atlas for study of pancreas biology and disease.
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Project description:Transgenic KrasG12D mice can recapitulate pancreas intra-epithelial neoplasia (PanIN). Caerulein is a cholecystokinin analogue and induces acute pancreatitis when injected intra-abdominally. Caerulein-induced acute pancreatitis will accelerate PanIN progression in KrasG12D mice. We compared mRNA profile changes between KrasG12D mice with acute caerulein-induced pancreatitis and wild-type mice without acute pancreatitis. The experiment had two groups. Experiment group: KrasG12D mice with acute caerulein-induced pancreatitis (N=6). Three mice in experiment group received 1-week caerulein injection, and the other three mice received 2-week caerulein injection. All experiment group mice started to receive caerulein injection at 1-month of age, and were sacrificed at the last day of caerulein injection. Control group: wild-type mice without acute pancreatitis (N=6). The mice were sacrificed at 1.5-month of age. Whole pancreas tissue lysate samples were subjected to mRNA array assay.
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