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Total RNA sequencing data of murine bone marrow derived macrophages from Apoe-/- and Apoe-/-/Treml4-/- mice stimulated with oxLDL

ABSTRACT: Total RNA sequencing data of murine bone marrow derived macrophages from Apoe-/- and Apoe-/-/Treml4-/- mice stimulated with oxLDL

PROVIDER: PRJNA607045 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11095831_1.fastq.gz	Fastqsanger.gz
	SRR11095831_2.fastq.gz	Fastqsanger.gz
	SRR11095832_1.fastq.gz	Fastqsanger.gz
	SRR11095832_2.fastq.gz	Fastqsanger.gz
	SRR11095833_1.fastq.gz	Fastqsanger.gz

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Total RNA sequencing data of murine bone marrow derived macrophages from Apoe-/- and Apoe-/-/Treml4-/- mice stimulated with oxLDL

Project description:Treml4 has been recently caracterized as a protein-coding gene of the Trem family. It has been shown that its expression is controlled by two cis- eQTL's and that the minor allele a these locuses confers up to 6.5 fold increased relative risk of human coronary arterial calcification (CAC). Since Treml4 expression is confined to the myeloid compartment, we aimed to, first, determined if Treml4 expression correlates with lipid laden macrophages and, second, investigate how gene expression is affected by Treml4 expression status utlizing a global knockdown mouse for Treml4 under the apolipoprotein deficient background.

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Total RNA sequencing data of murine bone marrow derived macrophages from WT and Treml4 deficient mice

Project description:Treml4 has been recently characterized as a protein-coding gene of the Trem family. It has been shown that its expression is controlled by two cis- eQTL's and that the minor allele a these locuses confers up to 6.5 fold increased relative risk of human coronary arterial calcification (CAC). Since Treml4 expression is confined to the myeloid compartment, we aimed to, first, determined if Treml4 expression correlates to inflammatory activation and, second, investigate how inflammatory gene expression is affected by Treml4 expression status utlizing a global knockdown mouse for Treml4.

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Project description:Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-loaded macrophages in the arterial wall. Intimal macrophages internalize modified lipoproteins such as oxidized LDL (oxLDL) through scavenger receptors, leading to storage of excess cholesteryl esters in lipid bodies and a "foam cell" phenotype. In addition, stimulation of macrophage Toll-like receptors (TLRs) has been shown to promote lipid body proliferation. We investigated the possibility that there are transcriptional regulators that are common to both pathways for stimulating foam cell formation (modified lipoproteins and TLR stimulation), and identified the transcription factor ATF3 as a candidate regulator. In this specific microarray experiment, we studied the effect of genetic knockout of ATF3 on the transcriptional response of macrophages to oxLDL. Murine bone marrow-derived macrophages from two different mouse strains (Atf3-/- and WT) were incubated in the presence or absence of oxidized low-density lipoprotein (oxLDL), and then transcriptionally profiled using the Affymetrix Mouse Exon Array 1.0 ST. The goal was to study the pattern of differential expression between WT and Atf3-/- strains, in oxLDL-induced foam cells and in non-foamy control cells, to identify cellular pathways that may be dysregulated under loss of the transcription factor ATF3 in macrophage foam cells. Twelve female mice (six Atf3-/-, and six WT control mice) were sacrificed at 8-12 weeks of age, and macrophages were derived from the femoral bone marrow using rhM-CSF. oxLDL was introduced into the medium for six samples (3 WT and 3 Atf3-/-) at 25 ug/mL on day seven, and after 24 h of incubation, RNA was isolated using Trizol. Labeled cRNA derived from the RNA samples was hybridized to Affymetrix Mouse Exon Array 1.0 ST GeneChips. Microarray data were processed using transcript-level probesets, and are in log2 scale.

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