Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA323726 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To directly test whether inhibition of IL-18 by IL-18 neutralizing monoclonal antibodies (IL-18 nAbs) is sufficient for blocking the inflammatory responses of heart caused by acute β-adrenergic insult, mice were subjected to intraperitoneal injection with rat IL-18 nAbs or IgG as a negative control 1hr after isoproterenol treatment.
2016-05-31 | GSE82034 | GEO
Project description:To further search for potential gene targets which are involved in the pathological process of myocardial infarction, we have employed whole genome microarray expression profiling as a discovery platform to identify the expression of STAT6, β1-adrenergic receptors and inflammatory cytokines. The CD11b+ cells were isolated from spleen and bone marrow of mice by magnetic beads, and the experimental mice were divided into four time points (control, MI 1week, MI 2 weeks, and MI 4 weeks). We found the β1-AR related sympathetic signal, the STAT6 signal and inflammatory cytokines (IL-1α, IL-18 and TGF-β) are involved in the activation of CD11b+ immune cells and cardiac fibrogenesis after myocardial infarction.
2020-11-16 | GSE154733 | GEO
Project description:Activated eosinophils is a major cell type to be involved in allergic diseases. Type 2 cytokines (IL-4 and IL-5) are important to establish and augment their inflammatory process. The aim of this study is to clarify the role of these cytokines as direct activators for human eosinophils.
2024-06-20 | PXD052200 | JPOST Repository
Project description:In immunosurveillance, bone-derived immune cells infiltrate the tumor and secrete inflammatory cytokines to destroy cancer cells. However, cancer cells have evolved mechanisms to usurp inflammatory cytokines to promote tumor progression. In particular, the inflammatory cytokine, interleukin-1 (IL-1), is elevated in prostate cancer (PCa) patient tissue and serum and promotes PCa bone metastasis. IL-1 also represses androgen receptor (AR) accumulation and activity in PCa cells, yet the cells remain viable; suggesting that IL-1 may also contribute to AR-targeted therapy resistance. Furthermore, IL-1 and AR protein levels negatively correlate in PCa tumor cells. Taken together, we hypothesize that IL-1 reprograms AR positive (AR+) PCa cells into AR negative (AR-) PCa cells that co-opt IL-1 signaling to ensure AR-independent survival in the inflammatory tumor microenvironment. Thus, we employed RNA sequencing to identify pathways that are modulated by IL-1 concomitant with IL-1-induced AR repression in PCa cells. Comparative analysis of sequencing data from the AR+ LNCaP PCa cell line versus the AR- PC3 PCa cell line reveals an IL-1-conferred gene suite in LNCaP cells that is constitutive in PC3 cells, and includes AR and AR target gene repression and the induction of prosurvival, lineage, and cancer stem cell genes. Bioinformatics analysis of the IL-1 regulated gene suite revealed that inflammatory and immune response pathways are primarily elicited; likely facilitating PCa cell survival in an inflammatory tumor microenvironment. Our data supports that IL-1 reprograms AR+ PCa cells to mimic AR- PCa gene expression patterns that favor AR-targeted treatment resistance and cell survival.
2018-02-01 | GSE105088 | GEO
Project description:Sympathetic overactivation under strong acute stresses triggers acute cardiovascular events including myocardial infarction (MI), sudden cardiac death, and stress cardiomyopathy. α1-ARs and β-ARs, two dominant subtypes of adrenergic receptors in the heart, play a significant role in the physiological and pathologic regulation of these processes. However, little is known about the functional similarities and differences between α1- and β-ARs activated temporal responses in stress-induced cardiac pathology. In this work, we systematically compared the cardiac temporal genome-wide profiles of acute α1-AR and β-AR activation in the mice model by integrating transcriptome and proteome. We found that α1- and β-AR activations induced sustained and transient inflammatory gene expression, respectively. Particularly, the overactivation of α1-AR but not β-AR led to neutrophil infiltration at 1 day, which was closely associated with the up-regulation of chemokines, activation of NF-κB pathway, and sustained inflammatory response. Furthermore, there are more metabolic disorders under α1-AR overactivation compared with β-AR overactivation. These findings provide a new therapeutic strategy that besides using β-blocker as soon as possible, blocking α1-AR within one day should also be considered in the treatment of acute stress associated cardiovascular diseases.
2023-01-19 | PXD036011 | Pride
Project description:During acute sympathetic stress, the overeactivation of β-adrenergic receptors (β-ARs) caused cardiac fibrosis, by triggering inflammation and cytokine expression. It is unknown whether exercise training inhibited acute β-AR overactivation-induced cytokine expression and cardiac injury. Here, we reported that running exercise inhibited cardiac fibrosis and improved cardiac function in mice treated by isoproterenol, a β-AR agonist. Cytokine antibody array revealed that exercise prevented the expression changes of most cytokines induced by isoproterenol. Specifically, 18 ISO-upregulated and 3 ISO-downregulated cytokines belonged to six families (eg. chemokine) were prevented. A further KEGG analysis of these cytokines revealed that Hedgehog and Rap1 signaling pathways were involved in the regulation of cytokine expression by exercise. The expression changes of some cytokines that were prevented by exercise were verified by ELISA and real-time PCR. In conclusion, running exercise prevented the cytokine changes following acute β-AR overactivation and therefore attenuated cardiac fibrosis.
2019-03-30 | GSE129022 | GEO
Project description:Aims: The sympathetic nervous system regulates numerous critical aspects of mitochondrial function in the heart through activation of adrenergic receptors (ARs) on cardiomyocytes. Chronic β-AR activation causes maladaptive alterations in cardiomyocyte metabolism that contribute to the pathobiology of heart failure. In contrast, mounting evidence suggests that a1-ARs, particularly the a1A subtype, are cardioprotective and may mitigate the deleterious effects of chronic β-AR activation by shared endogenous catecholamine ligands. The mechanisms through which a1A-ARs exert their cardioprotective effects remain unclear. Here we tested the hypothesis that a1A-ARs adaptively regulate cardiomyocyte oxidative metabolism in both the uninjured and failing heart.
Methods: We characterized the effects of global α1A-AR genetic deletion on mitochondrial function and metabolism in the uninjured mouse heart using high resolution respirometry, substrate-specific electron transport chain (ETC) enzyme assays, transmission electron microscopy (TEM), proteomics, and lipidomics. We then compared the effects of α1A- and β-AR agonist treatment on ETC enzyme activity and oxidative stress in vivo and in vitro. We subjected wild type and cardiomyocyte-specific α1A-KO mice to permanent left coronary artery (LCA) ligation and used RNAseq to compare the transcriptomic response. Results: We found that isolated cardiac mitochondria from mice with global α1A-AR genetic deletion (α1A-KO) had deficits in fatty acid-dependent respiration and ETC enzyme activity. TEM revealed abnormalities of mitochondrial morphology characteristic of these functional deficits. The selective α1A-AR agonist A61603 (100 ng/kg/d, 3d) enhanced fatty acid oxidation (FAO) in isolated cardiac mitochondria while increasing expression and activity of the mitochondrial trifunctional protein, a critical FAO mediator. The β-AR agonist isoproterenol enhanced oxidative stress in vitro and this adverse effect was mitigated by A61603. RNAseq revealed broad basal deficits in pathways related to mitochondria and OXPHOS in cardiomyocyte-specific α1A-KO mice; these differences were exaggerated by LCA ligation. A61603 enhanced ETC Complex I activity and protected contractile function following myocardial infarction.
Conclusions: Collectively, these novel findings position α1A-ARs as critical regulators of cardiomyocyte metabolism in the basal state and suggest that metabolic mechanisms may underlie the protective effects of α1A-AR activation in the failing heart.
2024-08-15 | PXD044591 | JPOST Repository
Project description:Background: Identifying the immune components that are regulated by a2NTD, a peptide cleaved from the N-terminus of the a2 vacuolar ATPase. Methods: In this study, we used pathway-focused PCR arrays to determine the genes that are regulated in human monocytic cell line, THP-1 after a2NTD stimulation over time. Results: a2NTD up-regulated several cytokines including IL-1 alpha, IL-1 beta, and IL-10. Several chemokines were also upregulated including the MCP and MIP families. Conclusion: We believe a2NTD to be an immune modulator made by tumor cells that aid in preventing immune surveillance by up-regulating proteins in monocytes that are both pro-and anti-inflammatory in nature. The Human Inflammatory Response and Autoimmunity RTM-BM-2 ProfilerM-bM-^DM-" PCR Array profiles the expression of 84 key genes involved in autoimmune and inflammatory immune responses. It represents the expression of inflammatory cytokines and chemokines as well as their receptors. It also contains genes related to the metabolism of cytokines and involved in cytokine-cytokine receptor interactions. Thoroughly researched panels of genes involved in the acute-phase response, inflammatory response, and humoral immune responses are represented as well. Using real-time PCR, you can easily and reliably analyze expression of a focused panel of genes related to inflammatory and autoimmune responses with this array.
2010-11-20 | E-GEOD-25490 | biostudies-arrayexpress
Project description:Interleukin-18 (IL-18) was one of the inflammatory cytokines and related to major depressive disorder (MDD) and dementia. Compared with Il18+/+ mice, IL-18 knockout (Il18−/−) mice developed impaired learning and memory, more anxiety, and less motivation. To reveal the mechanism, the microarray was performed.
2019-12-31 | GSE108485 | GEO
Project description:Analysis of MIN6 murine beta cell line transfected with Pla2g6 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.
2024-02-08 | PXD017863 | Pride