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accession-icon GSE56711
Mechanism of tissue-specific functional polarization of peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE56682
Genome wide transcriptional analysis of tissue macrophages and bone marrow derived macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Tissue macrophages from peritoneal cavity, lung, liver, spleen, small intestine and adipose tissue and M-CSF derived bone marrow derived macrophages (BMDMs) were determined for gene expression.

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP066776
Genome-wide analysis of chronic inflammation induced gene expression in livers isolated from either wild type or ApoE-Cyp7a1 transgenic animals.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Analysis of whole genome expression changes in livers from wild type animals and animals with a liver specific transgenic over expression of Cyp7a1. Mice were given a chronic, repetitive administration of LPS for 7 days. Our prior analysis had indicated that inflammation suppresses Cyp7a1 and that this leads to accumulation of intermediates in the mevalonate biosynthesis pathway. Here, we hypothesized that over expression of Cyp7a1 would not affect the changes in transcriptional state due to chronic administration of LPS. We provide gene expression data which evaluates this question. Here we find that over expression of Cyp7a1 minimally alters the transcriptome of livers in an untreated state, and that it has small effects on the response to chronic LPS. Overall design: Total RNA isolated from livers of wild type and liver specific Cyp7a1 transgenic animals treated with or without recurrent, daily LPS injections (1.5mg/kg) for 7 days. There are two biological replicates per condition. Samples are a matrix of all conditions reported as FPKMs.

Publication Title

The Effect of Sustained Inflammation on Hepatic Mevalonate Pathway Results in Hyperglycemia.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE56683
Gene induction by all trans retinoic acid (ATRA) and/or omentum culture supernatant in bone marrow derived macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

BMDMs were stimulated with ATRA and/or omentum culture supernatant and gene expression was determined by Illumina microarray

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE67422
Genome-wide analysis of chronic inflammation-induced gene expression in primary hepatocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of whole genome expression changes in primary hepatocytes in response to chronic stimulation with inflammatory cytokines. We hypothesized that chronic treatment of primary hepatocytes with TNF would result in a reprogramming of the cell's transcriptome to improve adaptation to the presence of a chronic inflammatory stress. Here we provide expression analysis detailing genes upregulated, downregulated, and unchanged after 2 days of TNF treatment. We have included gene expression profiling of cells treated with TNF for 2 hours to help isolate the changes unique to chronic TNF treatment of primary hepatocytes.

Publication Title

The Effect of Sustained Inflammation on Hepatic Mevalonate Pathway Results in Hyperglycemia.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE56684
GATA6 dependent gene regulation in peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Peritoneal macrophages from control and Mac-Gata6 KO (LysM-cre;Gata6-floxed) mice were determined for genome wide gene expression.

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE11698
Microarray of Trex1 WT and Trex1 KO hearts on RAG2KO background
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Heart ventricle tissue was harvested from Trex1/RAG2 DKO mice and from Trex1WT/RAG2KO littermate controls. RNA was extracted, and an Affymetrix Mouse 430 2.0 gene chip analysis was performed.

Publication Title

Trex1 prevents cell-intrinsic initiation of autoimmunity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE7348
Gene Expression in Naive and Tolerant Macrophages stimulated with LPS
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The inflammatory response initiated by microbial products signaling through Toll-like receptors (TLRs) of the innate immune system is essential for host defense against infection. Because inflammation can be harmful to host tissues, the innate response is highly regulated. Negative regulation of TLR4, the receptor for bacterial lipopolysaccharide (LPS), results in LPS tolerance, defined as hyporesponsiveness to repeated stimulation with LPS. LPS tolerance is thought to protect the host from excessive inflammation by turning off TLR4 signal, which then shuts down TLR-induced genes. However, TLR signaling induces hundreds of genes with very different functions. We reasoned that genes with different functions should have different requirements for regulation. Specifically, genes encoding proinflammatory mediators should be transiently inactivated to limit tissue damage, while genes encoding antimicrobial effectors, which directly target pathogens, should remain inducible in tolerant cells to protect the host from infection. Using an in vitro system of LPS tolerance in macrophages, here we show that TLR-induced genes may indeed be divided into two distinct categories based on their functions and regulatory requirements. Further, we show these distinct groups are regulated by gene-specific, and not signal-specific mechanisms.

Publication Title

Gene-specific control of inflammation by TLR-induced chromatin modifications.

Sample Metadata Fields

Specimen part

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accession-icon SRP052753
Two-signal requirement for growth-promoting function of Yap
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The transcriptional coactivator Yap promotes proliferation and inhibits apoptosis, suggesting that Yap functions as an oncogene. Most oncogenes, however, require a combination of at least two signals to promote proliferation. Here we present evidence that Yap activation is insufficient to promote growth in the otherwise normal tissue. Using a mosaic mouse model, we demonstrate that Yap overexpression in a fraction of hepatocytes does not lead to their clonal expansion, as proliferation is counterbalanced by increased apoptosis. To shift the activity of Yap towards growth, a second signal provided by tissue damage or inflammation is required. In response to liver injury, Yap drives clonal expansion, suppresses hepatocyte differentiation and promotes a progenitor phenotype. These results suggest that Yap activation is insufficient to promote growth in the absence of a second signal thus coordinating tissue homeostasis and repair. Overall design: Totally sixteen samples

Publication Title

Two-signal requirement for growth-promoting function of Yap in hepatocytes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP176476
Genome-wide RNA sequencing of sequential TLR agonist stimulation in C57Bl6/J macrophages
  • organism-icon Mus musculus
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report the genome-wide RNA sequencing of bone marrow derived macrophages after sequential TLR agonist stimulation. Overall design: Examination of sequential TLR agonist stimulation. Bone marrow derived macrophages (BMDMs) were prepared from male animals 6-12 weeks of age. Cells were isolated from femurs and tibias. The bone marrow cells were and grown in macrophage growth medium (RPMI 1640 supplemented with 10% FBS (Gibco), 1% penicillin-streptomycin (Gibco), 2 mM L-glutamine (Gibco), 1 mM sodium pyruvate (Gibco), 0.01 M HEPES (AmericanBio), and 30% L929-conditioned media as a source of CSF-1), and plated on petri dishes. Macrophage growth medium was supplemented on day 3. Cells were plated for use on day 6. For sequential stimuli, cells were first stimulated with, PBS, 100 ng/mL Poly I:C (InvivoGen), or 5 ng/mL LPS derived from Escherichia coli 055:B5 (Sigma-Aldrich). 24 hours after the initial stimulation, the media was removed and cells were washed twice with warmed macrophage growth media, and then the media was replaced with Poly I:C or LPS.

Publication Title

Specific sequences of infectious challenge lead to secondary hemophagocytic lymphohistiocytosis-like disease in mice.

Sample Metadata Fields

Specimen part, Cell line, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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