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: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:Tween-80 is one of the most important causes resulting in anaphylactoid reaction. However, its mechanism remains unclear. A Label-free LCMS/MS-based proteomics was used to analyze Tween-80-stimulated LAD2 mast cell releasates. Out of a total dataset of 2546 proteins, 882 proteins were found in the supernate samples of Tween-80-treated LAD2 mast cells; 313 proteins were up-expressed and 111 proteins were down-expressed. KEGG pathway analysis showed that endocytosis was the largest class of pathway. A total of 52 proteins were involved in endocytosis, and mainly related to G-protein-coupled receptor (GPCR)-endocytosis and EGFR-endocytosis. Cell adhesion molecules (CAMs) pathway was the most significant differences, with a total of 21 proteins involved. NF-κB signaling activation and calcium signaling pathway play an important role in Tween-80-induced LAD2 cells activation. Proteins, including tyrosine-protein kinase, PLCγ, PKCβ, and p50/p65, were mainly involved in NF-κB pathways. NF-κB signaling activation mainly involved in tyrosine-protein kinase, PLCγ, PKCβ, and NF-κB p50/p65. Calcium signaling pathway mainly related to PLCγ/PKC PLCγ/STIM1 mediated store-operated calcium entry (SOCE) and PLCγ mediated store-operated calcium entry (SOCE)PLCγ/PKC pathway. These results suggest that Tween-80 might be internalized via GPCR-endocytosis, which induces degranulation by SOCE PLCγ/PKC or SOCE PLCγ/PKC pathways mediated calcium influx, and promotes the generation of inflammatory mediators and CAMs via NF-κB signaling pathway finally resulting in anaphylactoid reaction.
2019-11-04 | PXD016123 | iProX
Project description:In this study, we generated knock-in CalExflox mice (Calcium Extrusion) for Cre-dependent expression of mCherry-hPMCA2w/b to attenuate astrocyte calcium signaling in genetically defined cells in vivo. We crossed CalExflox mice to astrocyte specific Aldh1l1-Cre/ERT2 mice in order to achieve inducible global CNS-wide calicum signaling attenuation. Within six days of induction in the bigenic mice, we observed profoundly altered ambulation in the open field, disrupted motor coordination and gait, and premature lethality, which based on imaging, behavioural, and RNA-seq analyses was likely to be partly due to significant cerebellar defects.
2021-07-14 | GSE164235 | GEO
Project description:Vesicular traffic and membrane contact sites between organelles enable the exchange of proteins, lipids, and metabolites. Recruitment of membrane tethers to contact sites between the endoplasmic reticulum (ER) and the plasma membrane is often triggered by calcium. In contrast, we reveal here a function for calcium in the repression of cholesterol export at membrane contact sites between the ER and the Golgi complex. We show that calcium efflux from ER stores induced by inositol-triphosphate [IP3] accumulation upon loss of the inositol 5-phosphatase INPP5A or sustained receptor signaling triggers the depletion of cholesterol and associated complex glycosphingolipids from the cell surface, resulting in a blockade of clathrin-independent endocytosis (CIE) of bacterial Shiga toxin. This phenotype is caused by the calcium-induced dissociation of oxysterol binding protein (OSBP) from the Golgi complex and from VAP-containing membrane contact sites. Our findings reveal a crucial function for INPP5A-mediated IP3 hydrolysis in the control of lipid exchange at membrane contact sites.
2021-05-06 | MTBLS2444 | MetaboLights