publication_authors:Ouimet M Results

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Microarray (72)

Rna-seq (15)

Platform

Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2) (39)

Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (33)

Illumina HiSeq 2000 (9)

Illumina HiSeq 2500 (6)

Includes Publication (15)

GSE47744

Molecular mechanisms vascular smooth muscle cell (VSMC) acquisition of macrophage features in response to cholesterol loading

Mus musculus
10 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In this study, murine primary aortic smooth muscle cells (SMCs) were transcriptionally profiled at baseline, after 3 d of cholesterol loading, and after 3 d of subsequent cholesterol unloading with HDL treatment, to identify vascular SMC genes that are transcripionally dysregulated in response to cholesterol loading and/or unloading.

Publication Title

Cholesterol loading reprograms the microRNA-143/145-myocardin axis to convert aortic smooth muscle cells to a dysfunctional macrophage-like phenotype.

Sample Metadata Fields

Age, Specimen part

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SRP100088

Transcriptional and accessible chromatin profiles during conversion process of alternatively activated macrophages (RNA-Seq)

Mus musculus
9 Downloadable Samples
Illumina HiSeq 2000

Description

Whether inflammatory macrophages can adopt features of the tissue resident niche and what mechanisms mediate phenotypic conversion remain unclear. In this study, we show by cell surface phenotyping, as well as by RNA-Seq transcriptional profiling and ATAC-Seq open chromatin regions profiling, that inflammatory monocyte can adopt a tissue resident phenotype, which is also accompanied by re-programming of the transcriptional profiles and remodeling of the open chromatin landscape. The conversion process is dependent on Vitamin A, suggesting that Vitamin A deficiency may lead to the failure to resolve inflammation, as inflammatory macrophages accumulate without adopting a tissue residency phenotype. Overall design: Monocyte-derived (N=3), tissue converted (N=3) and tissue resident (N=3) mouse peritoneal macrophages were FACS-sorted for RNASeq and ATACSeq.

Publication Title

Vitamin A mediates conversion of monocyte-derived macrophages into tissue-resident macrophages during alternative activation.

Sample Metadata Fields

Specimen part, Subject

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SRP103737

Expression analysis of genes modulated after knock-down of lncRNA CHROME.

Homo sapiens
6 Downloadable Samples
Illumina HiSeq 2500

Description

Thousands of long non-coding RNAs (lncRNAs) have been identified in the human genome, many of which are not conserved in lower mammals. The majority of these lncRNAs remain functionally uncharacterized and may have important implications in human physiology and disease. Here, we identify a primate-specific lncRNA, CHROME, which is increased in the plasma and atherosclerotic plaques of individuals with coronary artery disease compared to healthy controls. Using a loss-of-function approach, we show that CHROME functions as a competing endogenous RNA of microRNAs and regulates the concentration and biological functions of target genes. Overall design: We used three replicate samples of HEPG2 cells that were treated with shRNA for CHROME compated to three replicate control samples.

Publication Title

The long noncoding RNA CHROME regulates cholesterol homeostasis in primate.

Sample Metadata Fields

Specimen part, Cell line, Subject

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GSE9250

Genomic profiling in CLL and subtypes of del13q14

Homo sapiens
20 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Chronic lymphocytic leukemia (CLL) is a biologically heterogeneous illness with a variable clinical course. Loss of chromosomal material on chromosome 13 at cytoband 13q14 is the most frequent genetic abnormality in CLL, but the molecular aberrations underlying del13q14 in CLL remain incompletely characterized. We analyzed 171 CLL cases for LOH and sub-chromosomal copy loss on chromosome 13 in DNA from FACS-sorted CD19+ cells and paired buccal cells using the Affymetrix XbaI 50K SNP-array platform. The resulting high-resolution genomic maps, together with array-based measurements of expression levels of RNA in CLL cases with and without del13q14 and Q-PCR-based expression analysis of selected genes support the following conclusions: i) del13q14 is heterogeneous and composed of multiple subtypes with deletion of Rb or the miR15a/16 loci serving as anatomic landmarks, respectively ii) del13q14 type Ia deletions are relatively uniform in length and extend from breakpoints close to the miR15a/16 cluster to a newly identified telomeric breakpoint cluster at ~50.2-50.5 Mb physical position iii) LATS2 RNA levels are ~2.6-2.8-fold lower in cases with del13q14 type I that do not delete Rb as opposed to all other CLL cases and iv) ~15% of CLL cases display marked reductions in miR15a/16 expression often but not invariably associated with bi-allelic miR15a/16 loss. This data should aid future investigations into biological differences imparted on CLL by different del13q14 subtypes including investigations into LATS2 as one of the genes found deregulated as part of del13q14.

Publication Title

Integrated genomic profiling of chronic lymphocytic leukemia identifies subtypes of deletion 13q14.

Sample Metadata Fields

No sample metadata fields

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GSE57197

Functional roles of Acetylated Histone Marks at Mouse Meiotic Recombination Hotspots (expression)

Mus musculus
23 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Meiotic recombination is initiated by the Spo11 endonuclease, which directs DNA double strand breaks at discrete regions in the genome coined hotspots. Here we report the profiles and dynamics of histone modifications at the cores of mouse recombination hotspots in early meiotic prophase. To define the spectrum of possible regulators of histone methylation and acetylation at all stages of meiosis I, expression analyses of histone acetylases/deacetylases (HATs/HDACs) and and HMTs/HDMTs genes when comparing those expressed in spermatogonia, pre-leptotene and leptotene/zygotene versus pachytene meiotic stages.