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Transcriptional profiling of Regulatory T cells isolated from mice exposed to Smoke, Morphine and Smoke plus Morphine

ABSTRACT: Transcriptional profiling of Regulatory T cells isolated from mice exposed to Smoke, Morphine and Smoke plus Morphine

PROVIDER: PRJNA814223 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18277281_1.fastq.gz	Fastqsanger.gz
	SRR18277281_2.fastq.gz	Fastqsanger.gz
	SRR18277282_1.fastq.gz	Fastqsanger.gz
	SRR18277282_2.fastq.gz	Fastqsanger.gz
	SRR18277283_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of Regulatory T cells isolated from mice exposed to Smoke, Morphine and Smoke plus Morphine

Project description:Purpose: The goals of this study were to identify gene expression signatures that are unique to Tregs from mice upon treatments with smoke, morphine and smoke plus morphine Methods and results: Wild-type mice were treated with cigarette smoke (SM) for a period of eight weeks, and/or the chronic continuous administration of morphine (M) via mini-pumps for the final four weeks CD4+CD25highCD127low Tregs from spleen were purified by cell sorting to generate mRNA transcription. Transcriptional profiling revealed a unique Treg signatures in SM, M or SM + M relative to control mice. Conclusion: Our study represents the first detailed analysis of splenic Treg transcriptome in mice exposure to smoke plus morphine.

2022-04-14 | GSE198210 | GEO

Transcriptional profiling of Regulatory T cells isolated from mice exposed to Smoke, Morphine and Smoke plus Morphine

Project description:Transcriptional profiling of Regulatory T cells isolated from mice exposed to Smoke, Morphine and Smoke plus Morphine

| PRJNA814223 | ENA

NHBE exposed to cigarette smoke

Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course

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Effects of neonatal stress and morphine on murine hippocampal gene expression

Project description:Critically ill preterm infants experience multiple stressors while hospitalized. Morphine is commonly prescribed to ameliorate their pain and stress. We hypothesized that neonatal stress will have a dose-dependent effect on hippocampal gene expression, and these effects will be altered by morphine treatment. Male C57BL/6 mice were exposed to 5 treatment conditions between postnatal day 5 and 9: 1) Control, 2) mild stress + saline, 3) mild stress + morphine, 4) severe stress + saline and 5) severe stress + morphine. Hippocampal RNA was extracted and analyzed using Affymetrix Mouse Gene 1.0 ST Arrays. Single gene analysis and gene set analysis were used to compare groups with validation by qPCR. Stress resulted in enrichment of genes sets related to fear response, oxygen carrying capacity and NMDA receptor synthesis. Morphine downregulated gene sets related to immune function. Stress plus morphine resulted in enrichment of mitochondrial electron transport gene sets, and down-regulation of gene sets related to brain development and growth. We conclude that neonatal stress alone influences hippocampal gene expression, morphine alters a subset of stress-related changes in gene expression and influences other gene sets. Stress plus morphine show interaction effects not present with either stimulus alone. These changes may alter neurodevelopment. Male mice were exposed to 5 treatment conditions between postnatal day (P)5 and P9 (n=3/group), with birth recorded as P1. Litters were culled to n=7 maximum per dam. Groups included: 1) Untreated controls (CC), 2) mild stress + saline (MSS), 3) mild stress + morphine (MSM), 4) severe stress + saline (SSS) and 5) severe stress + morphine (SSM).

2013-08-30 | E-GEOD-50382 | biostudies-arrayexpress

Effects of neonatal stress and morphine on murine hippocampal gene expression

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Project description:Mammalian females are born with a finite number of non-renewing primordial follicles, the majority of which remain in a quiescent state for many years. Due to their non-renewing nature, these “resting” oocytes are particularly vulnerable to xenobiotic insult, resulting in premature ovarian senescence and the formation of dysfunctional oocytes. In this study we characterised the mechanisms behind cigarette smoke induced ovotoxicity, which is characterised by primordial follicle depletion. C57BL/6 5 week old female mice were exposed to cigarette smoke five times per week, for 12-18 weeks using a custom-designed and purpose-built nose-only, directed flow inhalation and smoke-exposure system. This was done in the hopes of gaining a better understanding of the mechanisms underpinning cigarette smoke induced ovotoxicity.

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