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RNA-seq of human monocytic cell line (THP-1) treated with compound #42, LPS, #42/LPS, or vehicle controls

ABSTRACT: RNA-seq of human monocytic cell line (THP-1) treated with compound #42, LPS, #42/LPS, or vehicle controls

PROVIDER: PRJEB43690 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5485320.fastq.gz	Fastqsanger.gz
	ERR5485330.fastq.gz	Fastqsanger.gz
	ERR5485340.fastq.gz	Fastqsanger.gz
	ERR5485350.fastq.gz	Fastqsanger.gz
	ERR5485360.fastq.gz	Fastqsanger.gz

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RNA-seq of human monocytic cell line (THP-1) treated with compound #42 (2D216), LPS, #42(2D216)/LPS, or vehicle controls

Project description:To explore the effects of compound #42 on RNA transcription of THP-1 cells, we performed RNA-seq analysis.

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Effect of p38 MAPK inhibitor SB203580 on gene expression in monocytic THP-1 cells stimulated with HIV gp120 or LPS.

Project description:Human monocytic THP-1 cells were exposed to HIV envelope protein gp120 or bacterial LPS in the presence and absence of a pharmacological inhibitor of the p38 mitogen-activated protein kinase (MAPK) for 4 and 24 hours. A microarray analysis was performed in order to assess differential gene expression at the RNA level. Human monocytic THP-1 cells were pre-treated for 15 min with 10 M-BM-5M SB203580 followed by exposure for 4 h or 24 h to 1 nM HIV gp120SF162 or 1 M-BM-5g/ml LPS. 0.1 % DMSO and 0.001 % BSA served as vehicle controls for SB203580 and gp120, respectively. The experimental samples were 1) control 4 h, 2) gp120 4 h, 3) LPS 4 h, 4) SB203580 (SB) 4 h, 5) SB+gp120 4 h, 6) SB+LPS 4 h, 7) control 24 h, 8) gp120 24 h, 9) LPS 24 h, 10) SB 24 h, 11) SB+gp120 24 h, 12) SB+LPS 24 h. RNA was isolated from three biological replicates for each experimental condition using an RNeasy kit commercially available from Qiagen (Valencia, CA). Roughly 2 X 106 cells were collected to obtain 500 ng M-bM-^@M-^S 2 M-BM-5g RNA. RNA quality (A260/A280 ratio ~1.8-2.0) was tested using the NanoDrop system from Thermo Scientific (Rockford, IL). High quality RNA was then provided to the Microarray/ QPCR Facility Core at Sanford-Burnham Medical Research Institute and DNA microarray was performed using the whole genome gene-expression analysis HumanHT-12 v4 Expression BeadChip kit from Illumina (San Diego, CA). Microarray results were further analyzed by Dr. Roy Williams (Bioinformatics Core, Sanford-Burnham Medical Research Institute) using the GeneSpring GX platform

2014-12-25 | E-GEOD-53712 | biostudies-arrayexpress

RNA-seq of human monocytic cell line (THP-1) treated with compound #1 or vehicle controls

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Effect of p38 MAPK inhibitor SB203580 on gene expression in monocytic THP-1 cells stimulated with HIV gp120 or LPS.

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Ribosome profiling (Ribo-Seq) and mRNA sequencing (RNA-Seq) of Human leukemia monocytic cell line (THP-1) cells upon treatment with LPS and LPS+dexamethasone (Dex).

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Project description:The objective of the study was to evaluate transcriptional response of endotoxin-stimulated human monocytic cells in presence or absence of host defense peptide LL-37 at low physiologically relevant concentrations. Human monocytic cells THP-1 were stimulated with LPS (10ng/ml) in presence or absence of LL-37 (5 ug/ml), as well as with the peptide alone, for 4 hours. The trends of LPS-induced altered gene expression in presence of the peptide were further validated by quantitative real-time PCR.

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RNA-seq analysis of PMA treament with or without LPS on human monocytic cell line THP1

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Identification of LPS-inducible genes down-regulated by ubiquinone in human THP-1 cells

Project description:Coenzyme Q10 (CoQ10) is an obligatory element in the respiratory chain and functions as a potent antioxidant of lipid membranes. More recently, anti-inflammatory effects as well as an impact of CoQ10 on gene expression have been observed. To reveal putative effects of Q10 on LPS-induced gene expression, whole genome expression analysis was performed in the monocytic cell line THP-1. 1129 probe sets have been identified to be significantly up-regulated (p < 0.05) in LPS-treated cells when compared to controls. Text mining analysis of the top 50 LPS up-regulated genes revealed a functional connection in the NFκB pathway and confirmed our applied in vitro stimulation model. Moreover, 33 LPS-sensitive genes have been identified to be significantly down-regulated by Q10-treatment between a factor of 1.32 and 1.85. GeneOntology (GO) analysis revealed for the Q10-sensitve genes a primary involvement in protein metabolism, cell proliferation and transcriptional processes. Three genes were either related to NFκB transcription factor activity, cytokinesis or modulation of oxidative stress. In conclusion, our data provide evidence that Q10 down-regulates LPS-inducible genes in the monocytic cell line THP-1. Thus, the previously described effects of Q10 on the reduction of pro-inflammatory mediators might be due to its impact on gene expression.

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