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Chromatin Capture Identifies SCARB1-LAG3 Proinflammatory Cardiovascular Disease Gene Networks [Hi-C]

ABSTRACT: Purpose: Utilized Next-generation sequencing (NGS) to profile global chromatin interaction differences between two populations, a selected carrier (C) alele of SNP (rs10846744) associated with cardiovascular disease (CVD) and a selected non-carrier (G) allele. Methods: Chromatin was isolated from two subjects, one homozygous for the rs10846744 reference (G) allele and one homozygous for the rs10846744 risk (C) allele, processed for dilution HiC (Lieberman-Aiden, van Berkum et al., 2009) and then subjected next-gen sequencing. Results: HiC-Pro integrated pipeline (with default parameters) was used for generating the HiC contact probability matrices (Servant et al., 2015). The results were visualized using HiCPlotter (Akdemir and Chin, 2015) and HiTC (Servant et al., 2012) and the Washington University EpiGenome Browser (Zhou and Wang, 2013). Juicebox (Durand et al., 2016) was utilized to extract observed/expected KR (Knight-Ruiz) normalized contacts for chromosome 12. Conclusions: Our study represents the first detailed analysis of significant changes in gene expression by an altered chromatin interaction network from SCARB1 to NR2F2 and LAG3, contributing to CAD proinflammatory gene networks.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110757 | GEO | 2019/10/04

REPOSITORIES: GEO

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Chromatin Capture Identifies SCARB1-LAG3 Proinflammatory Cardiovascular Disease Gene Networks [4C-Seq]

Project description:Purpose: Isolating chromatin interactions from a specific viewpoint, we utilized Next-generation sequencing (NGS) to profile specific chromatin interaction differences between two populations, a selected carrier (C) alele of SNP (rs10846744) associated with cardiovascular disease (CVD) and a selected non-carrier (G) allele. Methods: Chromatin was isolated from two subjects, one homozygous for the rs10846744 reference (G) allele and one homozygous for the rs10846744 risk (C) allele, processed for 4C-Seq (van de Werken et al., 2012). Results: 4C-ker (Raviram et al, 2016) analyzed the chromatin interaction data from the specific viewpoint. The results were visualized using the Washington University EpiGenome Browser (Zhou and Wang, 2013). Conclusions: Our study represents the first detailed analysis of significant changes in gene expression by an altered chromatin interaction network from SCARB1 to NR2F2 and LAG3, contributing to CAD proinflammatory gene networks.

2019-10-04 | GSE110752 | GEO

Chromatin Capture Identifies SCARB1-LAG3 Proinflammatory Cardiovascular Disease Gene Networks [ChIP-Seq]

Project description:Purpose: Using a selected carrier (C) allele of rs10846744 SNP associated with cardiovascular disease (CVD) and a selected non-carrier (G) allele, chromatin immunoprecipitation of a protein of interest, NR2F2, overexpressed and bound to the rs10846744 region in the risk (CC) cells was performed in triplicate. Methods: Using NR2F2 as the target protein, chromatin was immunoprecipitated from each cell type and subjected to Next-gen sequencing. Input controls for each cell type were also sequenced. Results: MACS (Zhang et al., 2008) was utilized for analysis. The narrow peak results were visualized using the Washington University EpiGenome Browser (Zhou and Wang, 2013) and bedgraph files were visualized in the Integrative Genomics Viewer (Thorvaldsdóttir et al., 2013) as bigwig files. Conclusions: Our study represents the first detailed analysis of significant changes in gene expression by an altered chromatin interaction network from SCARB1 to NR2F2 and LAG3, contributing to CAD proinflammatory gene networks.

2019-10-04 | GSE110756 | GEO

Chromatin Capture Identifies SCARB1-LAG3 Proinflammatory Cardiovascular Disease Gene Networks [RNA-Seq]

Project description:Purpose: Utilized Next-generation sequencing (NGS) to profile transcriptional differences between two populations, a selected carrier (C) alele of SNP (rs10846744) associated with cardiovascular disease (CVD) and a selected non-carrier (G) allele. Methods: RNA was isolated from three subjects homozygous for the rs10846744 reference (G) allele and three subjects homozygous for the rs10846744 risk (C) allele and then subjected to full transcriptome sequencing. Triplicates of one sample from each group were also sequences to overlay with chromatin data from each group. Knockdown of NR2F2 using lentiviral particles assessed differential expression between the treated and untreated risk replicates. The Illumina NextSeq 500 next gen sequencing platform (UCONN CGI, Storrs, CT) was used for RNA-Seq. HiSeq 2000 was used for biological replicates at Perkin Elmer. RNA targets of interest were validated by qPCR using TaqMan assays and proteins were blotted using standard western methodologies. Results: We normalized the raw read count by FPKM and using Cufflinks, identified differential transcripts. RNA-seq data confirmed differential expression of NR2F2 and LAG3, validated by qPCR. Conclusions: Our study represents the first detailed analysis of significant changes in gene expression by an altered chromatin interaction network from SCARB1 to NR2F2 and LAG3, contributing to CAD proinflammatory gene networks.

2019-10-04 | GSE108274 | GEO

Chromatin Capture Identifies SCARB1-LAG3 Proinflammatory Cardiovascular Disease Gene Networks

Project description:Increased high density lipoprotein (HDL) cholesterol levels have been associated with mutations in the cholesterol efflux receptor gene SCARB1, contributing to coronary artery disease (CAD). Using chromatin capture techniques (4C-Seq and HiC), ChIP-Seq and RNA-Seq, we identified a potential mechanism between a non-coding SNP (rs10846744) within the first intron of SCARB1 and LAG3, a negative regulator of T cells, both on chromosome 12. We previously demonstrated how loss of LAG3 is associated with inflammation and CAD found in carriers of the rs10846744 risk allele (C) both in our hyperalphalipoproteinemia (HALP) participants and the Multi-Ethnic Study of Atherosclerosis (MESA), increasing the risk of a coronary event by 45% (PMID: 27777974). NR2F2 transcription factor binding, as detected by (yeast 1 hybrid assay, ChIP, and ChIP-Seq) to the rs10846744 risk (C) allele, bridges NR2F2, SCARB1, and LAG3 loci, altering gene networks associated with a CAD proinflammatory signature. This SuperSeries is composed of the SubSeries listed below.

2019-10-04 | GSE110761 | GEO

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Project description:Col-0 transgenic plants expressing MSH1P::FLAG::RPL18 were generated in both msh1 homozygous mutant (SAIL-877-F01) and wild type backgrounds with cloned MSH1 sequence described in Xu et al. (2011) and with transformation by the floral dip method (Clough and Bent, 1998). Positive transgenic lines were screened for FLAG tag by immunoblotting methods. Polysomal mRNA from MSH1-specific cells was obtained by ribosome purification using the TRAP method essentially as reported by (Reynoso et al., 2015) from floral stem tissues.

2018-12-26 | GSE114199 | GEO

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Project description:Purpose: Utilized Next-generation sequencing (NGS) to profile transcriptional differences between two populations, carriers (CC) of rs10846744 SNP associated with cardiovascular disease (CVD) and non-carriers (GG) who are disease free. Methods: Total RNA was isolated from three subjects homozygous for the rs10846744 reference (GG) allele and three subjects homozygous for the rs10846744 risk (CC) allele and then subjected to full transcriptome sequencing using the Perkin Elmer next gen sequencing platform (Perkin Elmer, Branford, CT). Bioinformatics was performed using Perkin Elmer GeneSifter software program. The data was adjusted by selecting total map reads, quality reads >20, log transformation, and using Benjamini Hochberg to correct for multiple testing. RNA targets of interest were validated by qRT–PCR using TaqMan assays and western blotting using standard methodologies. Results: Using Perkin Elmer's Genesifter Analysis Edition Software, we mapped about 100 million sequence reads per sample to the human genome (build 37.2), normalized the raw read count by total mapped million reads and identified 937 upregulated and 587 downregulated transcripts in the EBV (Epstein Barr Virus)-transformed B lymphocyte cells isolated from 3 carriers of the risk (CC) allele and 3 non-carriers of the (GG) reference allele with BWA workflow. RNA-seq data confirmed differential expression of LAG3 and this was validated with qRT–PCR. Conclusions: Our study represents the first detailed analysis of differential LAG3 expression, contributing to CVD, with biologic replicates, generated by RNA-seq technology.

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Project description:RNA-sequencing data from human iPSC PGP1 cells (n=4) differentiated into mesoderm (day-2) (n=4) or cardiomyocytes (days 25-30) (n=4) through modulation of Wnt/β-catenin signaling as previously described (Cohn et al., 2019; Hinson et al., 2017; Hinson et al., 2015; Lian et al., 2012).

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Project description:A previous study has shown that PML-dependent recruitment of HIRA to ISG promoters contributes to the up-regulation of gene expression as a result of cytokine release in response to HSV infection (McFarlane et al., 2019). Although carried out in non-neuronal cells, this study and others (Ulbricht et al., 2012, Kim and Ahn, 2015, Scherer et al., 2016, Chen et al., 2015) suggest that PML itself may contribute to ISG upregulation, so to determine whether PML was indeed required for ISG stimulation in SCG neurons, we carried out RNA sequence analysis in IFNα-treated neurons depleted of PML.

2021-06-21 | GSE166738 | GEO

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