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Homo sapiens

ABSTRACT: Integrative DNA, RNA and protein evidence connects TREML4 to coronary artery calcification

PROVIDER: PRJNA251404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1313290_1.fastq.gz	Fastqsanger.gz
	SRR1313290_2.fastq.gz	Fastqsanger.gz
	SRR1313300_1.fastq.gz	Fastqsanger.gz
	SRR1313300_2.fastq.gz	Fastqsanger.gz
	SRR1313291_1.fastq.gz	Fastqsanger.gz

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Integrative DNA, RNA and protein evidence connects TREML4 to coronary artery calcification

2014-06-10 | GSE58150 | GEO

Integrative DNA, RNA and protein evidence connects TREML4 to coronary artery calcification

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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: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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RNA-seq of human PBMC's and blood derived macrophages from healthy donors carrying the common (non permissive Treml4 expression) or minor (permissive Treml4 expression) allele for rs2803496 which controls Treml4 expression

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, determine if Treml4 expression correlates to inflammatory activation and, second, investigate how inflammatory gene expression is affected by Treml4 expression status in donors carrying the minor allele for a rs2803496.

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Project description:Objective – Vascular calcification is a critical pathology associated with increased cardiovascular event risk, but there are no FDA-approved anti-calcific therapies. We hypothesized and validated that an unbiased screening approach would identify novel mediators of human vascular calcification. Approach and Results – We performed an unbiased quantitative proteomics and pathway network analysis that identified increased carnitine O-octanoyltransferase (CROT) in calcifying primary human coronary artery smooth muscle cells (SMCs). Additionally, human carotid artery atherosclerotic plaques contained increased immunoreactive CROT near calcified regions. CROT siRNA reduced fibrocalcific response in calcifying SMCs. In agreement, histidine 327 to alanine point mutation inactivated human CROT fatty acid metabolism enzymatic activity and suppressed SMC calcification. CROT siRNA restored mitochondrial proteome alterations and suppressed mitochondrial fragmentation in calcifying SMCs. Lipidomics analysis of SMCs incubated with CROT siRNA revealed increased eicosapentaenoic acid, a vascular calcification inhibitor. CRISPR/Cas9-mediated Crot deficiency in low-density lipoprotein receptor-deficient mice reduced aortic and carotid artery calcification without altering bone density, or liver and plasma cholesterol and triglyceride concentrations. Conclusions – CROT is a novel inducer of vascular calcification via promoting fatty acid metabolism and mitochondrial dysfunction, as such CROT inhibition has strong potential as an anti-fibrocalcific therapy.

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