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Actication of alpha7 nicotinic receptor regulates herpes simplex virus infection in the central nervous system

ABSTRACT: mRNA isolated from a mouse microglia cell line, BV2 cells, treated with or without α7 nicotinic receptor agonist, choline, before HSV-1 infection. mRNA expression was examined with the NanoString© platform (www.nanostring.com) utilizing the Mouse Neuropatholgy codeset (NS_Mm_neuropath_V1.0) that measures 760 endogenous and 10 housekeeping (HK) RNAs.

ORGANISM(S): Mus musculus

PROVIDER: GSE252868 | GEO | 2024/06/24

REPOSITORIES: GEO

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Activation of alpha7 nicotinic receptor regulates herpes simplex virus infection in the central nervous system

Project description:mRNA isolated from a mouse microglia cell line, BV2 cells, treated with or without α7 nicotinic receptor agonist PNU-282987 before HSV-1 infection. mRNA expression was examined with the NanoString© platform (www.nanostring.com) utilizing the Mouse Neuropatholgy codeset (NS_Mm_neuropath_V1.0) that measures 760 endogenous and 10 housekeeping (HK) RNAs.

2024-06-24 | GSE252930 | GEO

α7 nicotinic acetylcholine receptor signaling modulates the inflammatory phenotype of fetal brain microglia: first evidence of interference by iron homeostasis.

Project description:We sequenced mRNA from 7 microglia extracted from sheep fetuses exposed to LPS, agonist and antagonist of α7 nicotinic acetylcholine receptor to determine signaling pathway through modeling of α7 during inflammation.

2017-08-11 | GSE101857 | GEO

Activation of alpha7 nicotinic receptor regulates herpes simplex virus infection in the central nervous system.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-24 | GSE252931 | GEO

Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

Project description:Purpose: The goal of this study is to compare the effects of inhaled nicotine on aortic gene expression and the role of the alpha7 nicotinic acetylcholine receptor (alpha7-nAChR) in mediating the nicotine effects. Methods: WT and alpha7-nAChR knockout (KO) mice at 5-month of age were exposed to nicotine vapor or room air for a total of 12 weeks. Total RNA was extracted from thoracic aortas using RNeasy Plus mini kit followed by library preparation using SMART-Seq v4 Ultra Low Input RNA Kit. Illumina next generation sequencing was performed using the NextSeq 500 system with the high output flow cell (up to 800 M paired end reads). Results: A total of 179 differentially expressed genes (149 upregulated and 30 downregulated, adjusted P-value < 0.1) were found in thoracic aortas from WT mice exposed to nicotine vapor compared to those exposed to room air. In contrast, only 7 non-overlapping genes were found to be differentially expressed in alpha7-nAChR KO mice exposed to nicotine compared to the air controls. Conclusions: Our study suggests that nicotine-induced changes in vascular gene expression is largely mediated by the alpha7-nAChR.

2022-02-08 | GSE196184 | GEO

Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

Project description:Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

| PRJNA803731 | ENA

α7 nicotinic acetylcholine receptor signaling modulates fetal sheep brain astrocytes transcriptome in response to endotoxin stress: comparison to microglial transcriptome and implications for autism spectrum disorder

Project description:Neuroinflammation in utero may result in lifelong neurological disabilities. Astrocytes play a pivotal role, but the mechanisms are poorly understood. No early postnatal treatment strategies exist to enhance neuroprotective potential of astrocytes. We hypothesized that agonism on α7 nicotinic acetylcholine receptor (α7nAChR) in fetal astrocytes will augment their neuroprotective transcriptome profile, while the antagonistic stimulation of α7nAChR will achieve the opposite. Using an in vivo - in vitro model of developmental programming of neuroinflammation induced by lipopolysaccharide (LPS), we validated this hypothesis in primary fetal sheep astrocytes cultures re-exposed to LPS in presence of a selective α7nAChR agonist or antagonist. Our RNAseq findings show that a pro-inflammatory astrocyte phenotype acquired in vitro by LPS stimulation is reversed with α7nAChR agonistic stimulation. Conversely, antagonistic α7nAChR stimulation potentiates the pro-inflammatory astrocytic phenotype. Furthermore, we conduct a secondary transcriptome analysis against the identical α7nAChR experiments in fetal sheep primary microglia cultures and against the Simons Simplex Collection for autism spectrum disorder and discuss the implications.

2019-04-29 | GSE123713 | GEO

whole brains from nicotinic acetylcholine receptor subunit mutant mice and littermate controls

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor

2006-09-22 | GSE5320 | GEO

Herpes simplex host shutoff attenuates antiviral state

Project description:Herpes simplex virus mutants lacking the vhs gene are severely attenuated in animal models of pathogenesis and exhibit reduced growth in primary cell culture. As a result of these properties vhs-deleted virus have been proposed as live-attenuated viruses. Despite these findings and their implications for vacccines, the mechanisms by which vhs promotes infection in cell culture and in vivo are not understood. In this study we demonstrate that vhs-deficent viruses replicate to reduced levels in interferon(IFN)- primed cells. Furthermore, vhs-defective viruses induce increased levels of IFN? and IFN?-stimulated genes, and increased levels of eIF2? phosphorylation in infected cells. In addition, we demonstrate a generalized over-expression of viral RNAs following infection with a vhs-deficient virus. This suggests increased expression of IFN pathway inducing double stranded RNA, a potent pathogen-associated molecular pattern (PAMP). Together these data show that vhs likely functions to reduce innate immune responses and thereby acts as critical determinant of viral pathogenesis. Keywords: time course, genetic modification Time course (1,3,6,9 & 12h) of HSV infected mouse embryo fibroblasts. Wild type (KOS) virus is co-hybridized with vhs null virus (NHB). Each time-point is hybridized in quadruplicate.

2008-04-03 | E-GEOD-10962 | biostudies-arrayexpress

Transcription profiling of Bordetella bronchiseptica RB50 nicotinic acid dose curve

Project description:B. bronchiseptica RB50 and a constitutive Bvg+ phase-locked mutant were grown at 37 degrees C in media containing a range of nicotinic acid concentrations.

2006-03-31 | E-TABM-28 | biostudies-arrayexpress

Transcriptional profile changes in retinal pigment epithelial cell culture after treatment with an α7 nicotinic acetylcholine receptor agonist

Project description:Transcriptional profile changes in retinal pigment epithelial cell culture after treatment with an α7 nicotinic acetylcholine receptor agonist

| PRJNA658979 | ENA

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