Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151907 | ENA |
REPOSITORIES: ENA
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Project description:Inflammation features in diverse central nervous system disorders such as stroke, trauma, neurodegeneration, infection and autoimmunity. To better understand how inflammatory mediators may alter astrocyte functions, we examined the effects of transforming growth factor-β1 (TGF-β1), lipopolysaccharide (LPS) and interferon-gamma (IFNγ) on purified, murine, primary cortical astrocyte cultures. We used microarrays to conduct whole genome expression profiling, and measured calcium signaling, which is implicated in mediating dynamic astrocyte functions. Combinatorial exposure to TGF-β1, LPS and IFNγ significantly modulated astrocyte expression of over 6,800 genes and resulted in both additive and synergistic changes compared with individual stimuli alone. Bioinformatic analysis revealed that combinatorial treatment significantly and markedly up regulated molecular networks and pathways associated with immune signaling and with regulation of cell compromise, death, growth and proliferation. These findings provide databases of astrocyte transcriptome changes elicited by the inflammatory stimuli, TGF-β1, LPS and IFNγ alone and in combination, and show that these stimuli up regulate astrocyte molecular networks associated with immune- and injury-related functions and significantly alter astrocyte calcium signaling evoked by multiple GPCR. We used microarrays to examine the effects of transforming growth factor-β1 (TGF-β1), lipopolysaccharide (LPS) and interferon-gamma (IFNγ) on purified, murine, primary cortical astrocyte cultures.
2012-10-18 | E-GEOD-36089 | biostudies-arrayexpress
Project description:Inflammation features in diverse central nervous system disorders such as stroke, trauma, neurodegeneration, infection and autoimmunity. To better understand how inflammatory mediators may alter astrocyte functions, we examined the effects of transforming growth factor-β1 (TGF-β1), lipopolysaccharide (LPS) and interferon-gamma (IFNγ) on purified, murine, primary cortical astrocyte cultures. We used microarrays to conduct whole genome expression profiling, and measured calcium signaling, which is implicated in mediating dynamic astrocyte functions. Combinatorial exposure to TGF-β1, LPS and IFNγ significantly modulated astrocyte expression of over 6,800 genes and resulted in both additive and synergistic changes compared with individual stimuli alone. Bioinformatic analysis revealed that combinatorial treatment significantly and markedly up regulated molecular networks and pathways associated with immune signaling and with regulation of cell compromise, death, growth and proliferation. These findings provide databases of astrocyte transcriptome changes elicited by the inflammatory stimuli, TGF-β1, LPS and IFNγ alone and in combination, and show that these stimuli up regulate astrocyte molecular networks associated with immune- and injury-related functions and significantly alter astrocyte calcium signaling evoked by multiple GPCR.
2012-10-18 | GSE36089 | GEO
Project description:Mast cells are tissue-resident immune cells that are critical for the pathogenesis of allergic and inflammatory disorders. Their physiological functions include host defense against parasites and, more recently, food quality control through antigen avoidance. The purine nucleoside adenosine (ADO), like other mast cell activators, such as antigens or Mrgprb2 agonists, increases intracellular Ca2+ concentration; however, it fails to induce degranulation of preformed mediators when applied to mast cells alone, and there is limited knowledge of whether ADO evokes the de novo synthesis and release of inflammatory mediators in tissue mast cells. An unbiased genome-wide analysis of gene expression triggered by various mast cell activators should enable identification of the gene program specifically activated by ADO in mast cells and thereby reveal new components of the associated inflammatory responses. Here, we performed bulk RNA sequencing in primary murine peritoneal mast cells (PMCs) as connective tissue mast cells. By comparing responses evoked by ADO stimulation with those of the Mrgprb2 agonist compound 48/80 and antigens activating FcεRI receptors, we identified 393 genes uniquely regulated by ADO, including genes encoding the de novo synthesized mediators transforming growth factor α and interleukin 7. Transcription factor activity inference, protein classification, functional enrichment analysis, protein interaction network, and topology analysis revealed a distinct ADO-specific transcriptional gene program involved in phosphoinositide signaling, vesicle trafficking, glycolysis, mitochondrial activity, and cell cycle arrest. The functional relevance of the identified de novo synthesized mediators for ADO-evoked inflammatory reactions can be evaluated in future studies.
2026-03-10 | GSE324337 | GEO
Project description:Protein kinase A is a downstream effector of many inflammatory mediators that induce pain hypersensitivity by increasing the mechanosensitivity of nociceptive sensory afferent. Here we examine the molecular mechanism underlying protein kinase-Adependent modulation of the mechanically-activated ion channel PIEZO2, which confers mechanosensitivity to many nociceptors. Using phosphorylation site prediction algorithms, we identified multiple putative and highly conserved PKA phosphorylation sites located on intracellular intrinsically disordered regions of PIEZO2. Site-directed mutagenesis and patch-clamp recordings showed that substitution of one or multiple putative PKA sites within a single intracellular domains does not alter PKA-induced PIEZO2 sensitization, whereas mutation of a combination of nine putative sites located on four different intracellular regions completely abolishes PKA-dependent PIEZO2 modulation, suggesting that the effect requires multisite phosphorylation. By demonstrating that PIEZO1 is not modulated by PKA, our data also reveals a previously unrecognized functional difference between PIEZO1 and PIEZO2. Moreover, by demonstrating that PKA only modulates PIEZO2 currents evoked by focal mechanical indentation of the cell, but not currents evoked by pressure-induced membrane stretch, we provide evidence suggesting that PIEZO2 is a polymodal mechanosensor that engages different protein domains for detecting different types of mechanical stimuli.
2023-07-20 | PXD041372 | Pride
Project description:Astrocyte responses to neuronal injury may be beneficial or detrimental to neuronal recovery, but the mechanism that determines these different responses are poorly understood. Transcriptional analysis showed that EphB1 induces a protective inflammatory signature in astrocytes, which is distinct from the response evoked by interleukin (IL)-6, which is known to have both pro- and anti-inflammatory properties. We demonstrate that this beneficial EphB1 induced signaling pathway is disrupted in astrocytes derived from human induced pluripotent stem cells (iPSC) of amyotrophic lateral sclerosis (ALS) patients.
2017-09-01 | GSE102903 | GEO
Project description:Astrocyte responses to neuronal injury may be beneficial or detrimental to neuronal recovery, but the mechanism that determines these different responses are poorly understood. Transcriptional analysis showed that EphB1 induces a protective inflammatory signature in astrocytes, which is distinct from the response evoked by interleukin (IL)-6, which is known to have both pro- and anti-inflammatory properties. We demonstrate that this beneficial EphB1 induced signaling pathway is disrupted in astrocytes derived from human induced pluripotent stem cells (iPSC) of amyotrophic lateral sclerosis (ALS) patients.
2017-09-01 | GSE102902 | GEO
Project description:We used microarrays to investigate if keratinocytes excert an immuno-inflammatory response towards M1 protein. Keratinocytes respond to M1 protein by activating pathways to induce the production of inflammatory signaltransducers, AP-1 and NFkB transcription factor subunits together with inflammatory mediators such as IL-8, CCL20 and IL-1 family proteins etc. HaCaT cells were cultured in serum-free media, without calcium, until 80% confluency. Cells were incubated in absence or presence of M1 protein before RNA extraction. The integrity of RNA quality was analysed by an Bioanalyzer. Out of 12 samples, 3 M1 stimulated and 3 control samples were chosen for hybridization on Affymetrix Human 2.0 ST array.
2014-10-03 | E-GEOD-61993 | biostudies-arrayexpress
Project description:Epidermal keratinocytes are key for maintenance of the integrity of the epidermis. One of the main drivers of keratinocyte differentiation is the calcium gradient; calcium concentration gradually increases towards the outer layers of the epidermis. Atopic dermatitis (AD) is a disorder associated with a chronic inflammatory state and a compromised epidermal barrier. Keratinocytes secrete lipid-rich small extracellular vesicles (sEVs) that acts as mediators of both local and long-distance signaling.
2022-06-07 | PXD031729 | Pride
Project description:Astrocyte glucocorticoid receptor signaling restricts neuronal plasticity
| PRJNA1310302 | ENA
Project description:The trigeminal nerve is primarily responsible for facial sensation and exhibits the highest expression of CGRP. Here, we explored the impact of Rimegepant on the transcriptome of the trigeminal ganglion in mice and found that the transcription profiles changed significantly following treatment compared to the control group. Following Rimegepant administration, we observed a significant downregulation of innate immune-related items within the trigeminal ganglia, as well as functional items directly associated with pain perception and calcium signaling pathways.The activation of innated immune within the trigeminal ganglia is known to enhance nociceptive responses, which were also directly linked to the activation of calcium signaling pathways. These results suggest that Rimegepant alleviates OSCC-related pain by mitigating the inflammatory condition within the trigeminal ganglion. We then categorized the genes enriched in these functional groups. Genes that promote the proliferation and differentiation of innate immune cells, and those related to the expression of proinflammatory mediators, were significantly downregulated, while those associated with anti-inflammatory functions were significantly upregulated. Additionally, genes from various chemokine receptor families and ion channel genes linked to neuronal activity were significantly downregulated. Collectively, these results suggest that CGRP influences OSCC-related pain by modulating the innate immune status of the trigeminal nerve.
2026-03-01 | GSE260740 | GEO