BMDM treated with I-BET151 and sitmulated with IgG immune complex
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA822764 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18587911_1.fastq.gz | Fastqsanger.gz | |||
| SRR18587911_2.fastq.gz | Fastqsanger.gz | |||
| SRR18587912_1.fastq.gz | Fastqsanger.gz | |||
| SRR18587912_2.fastq.gz | Fastqsanger.gz | |||
| SRR18587913_1.fastq.gz | Fastqsanger.gz |
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Project description:BMDC treated with I-BET151 and sitmulated with IgG immune complex
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Project description:The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury.
2012-04-04 | GSE27642 | GEO
Project description:The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury. MH.S-miR127 and MH.S-Sico cells were cultured for RNA extraction.Total RNA were assessed for quality with Agilent 2100 Bioanalyzer G2939A (Agilent Technologies,Santa Clara, CA)) and Nanodrop 8000 spectrophotometer (Thermo Scientific/Nanodrop, Wilmington, DE). Hybridization targets were prepared with MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems/Ambion, Austin, TX) from total RNA, hybridized to GeneChip® Mouse Genome 430 2.0 arrays in Affymetrix GeneChip® hybridization oven 645, washed in Affymetrix GeneChip® Fluidics Station 450 and scanned with Affymetrix GeneChip® Scanner 7G according to standard Affymetrix GeneChip® Hybridization, Wash, and Stain protocols. (Affymetrix, Santa Clara,CA).
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Project description:Mouse bone marrow-derived macrophages (BMDM) grown in macrophage colony-stimulating factor (CSF-1) have been used widely in studies of macrophage biology and the response to toll-like receptor agonists. We investigated whether similar cells could be derived from the domestic pig. Cultivation of pig bone marrow cells for 5-7 days in presence of rhCSF-1 generated a pure population of BMDM that expressed the usual macrophage markers (CD14, CD16, CD163, CD172a), are potent phagocytic cells and produced tumor necrosis factor (TNF) in response to lipopolysaccharide (LPS). Bone marrow cells could be stored frozen and thawed, providing a renewable resource. We profiled gene expression in pig BMDM from outbred animals (Large-White Landrace F1cross) responding to LPS using Affymetrix microarrays. The temporal cascade of inducible and repressible genes more closely-resembled human than mouse macrophages, and included genes involved in tryptophan metabolism (IDO, KYN), lymphoattractant chemokines (CCL20) and the vitamin D3-converting enzyme Cyp27B1. Conversely, pig BMDM, like human macrophages, did not induce genes involved in arginine metabolism, nor did they produce nitric oxide. The data establish pig BMDM as an alternative tractable model for the study of macrophage transcriptional control. RNA for gene expression analysis was collected at time points 0, 2, 7 and 24 hours post LPS stimulation (100ng/ml). Each time point included BMDM from the same three pigs and each cell culture was replicated. The replicate of the pig3_24h was not suitable for RNA analysis. Therefore, a total of 23 microarrays were hybridized.
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Project description:Mouse bone marrow-derived macrophages (BMDM) grown in macrophage colony-stimulating factor (CSF-1) have been used widely in studies of macrophage biology and the response to toll-like receptor agonists. We investigated whether similar cells could be derived from the domestic pig. Cultivation of pig bone marrow cells for 5-7 days in presence of rhCSF-1 generated a pure population of BMDM that expressed the usual macrophage markers (CD14, CD16, CD163, CD172a), are potent phagocytic cells and produced tumor necrosis factor (TNF) in response to lipopolysaccharide (LPS). Bone marrow cells could be stored frozen and thawed, providing a renewable resource. We profiled gene expression in pig BMDM from outbred animals (Large-White Landrace F1cross) responding to LPS using Affymetrix microarrays. The temporal cascade of inducible and repressible genes more closely-resembled human than mouse macrophages, and included genes involved in tryptophan metabolism (IDO, KYN), lymphoattractant chemokines (CCL20) and the vitamin D3-converting enzyme Cyp27B1. Conversely, pig BMDM, like human macrophages, did not induce genes involved in arginine metabolism, nor did they produce nitric oxide. The data establish pig BMDM as an alternative tractable model for the study of macrophage transcriptional control.
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