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accession-icon SRP096073
Gene expression profiling of human MSC-educated macrophages vs. classical macrophages from bone marrow and blood
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In comparison to MØs, MEMs have increased expression of the inhibitory molecules PD-L1, PD-L2, in addition to markers of alternatively activated macrophages: CD206 and CD163. RNA-Seq analysis of MEMs, as compared to MØs, show a distinct gene expression profile that positively correlates with multiple pathways important in tissue repair. MEMs also show increased expression of IL-6, TGF-ß, Arginase-1, CD73, and decreased expression of IL-12 and TNF-a. We show that IL-6 secretion is controlled in part by the COX-2, arginase and JAK1/STAT1 pathway. When tested in vivo, we show that human MEMs significantly enhance survival from lethal GVHD, and improve survival of mice from radiation injury. Overall design: Human macrophages were isolated from PBMCs and then exposed to MSCs. RNA was isolated then subjected to RNA-Seq.

Publication Title

Human Mesenchymal Stem Cell-Educated Macrophages Are a Distinct High IL-6-Producing Subset that Confer Protection in Graft-versus-Host-Disease and Radiation Injury Models.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE7491
Expression data from rat lung alveolar development
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Lung alveolarization is a complex process that involves interactions between several cell types and leads to considerable increase in gas-exchange surface area. The step designated secondary septation includes elastogenesis from interstitial fibroblasts.

Publication Title

Gene expression profiling in lung fibroblasts reveals new players in alveolarization.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE71124
Out-of-Sequence Signal 3 Paralyzes Primary CD4+ T Cell Dependent Immunity
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Primary T cell activation involves the integration of three distinct signals delivered in sequence: 1) antigen recognition, 2) costimulation, and 3) cytokine-mediated differentiation and expansion. Strong immunostimulatory events such as immunotherapy or infection induce profound cytokine release causing bystander T cell activation, thereby increasing the potential for autoreactivity and need for control. We show that during strong stimulation, a profound suppression of primary CD4+ T cell-mediated immune responses ensued and was observed across preclinical models and patients undergoing high-dose interleukin-2 (IL-2) therapy. This suppression targeted nave CD4+ but not CD8+ T cells and was mediated through transient suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor signaling pathway. These events resulted in complete paralysis of primary CD4+ T cell activation affecting memory generation, induction of autoimmunity, as well as impaired viral clearance. These data highlight the critical regulation of nave CD4+ T cells during inflammatory conditions.

Publication Title

Out-of-Sequence Signal 3 Paralyzes Primary CD4(+) T-Cell-Dependent Immunity.

Sample Metadata Fields

Treatment

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accession-icon SRP068591
Gene signature in sessile serrated polyps identifies colon cancer subtype
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

RNA sequencing analysis of gene expression in serrated colon polyps, uninvolved colon and control colon Overall design: 86 colon RNA sequencing datasets (21 sessile serrated adenomas/polyps, 10 hyperplastic polyps, 10 adenomatous polyps, 21 uninvolved colon, 20 control colon and 4 colon cancer)

Publication Title

Gene Signature in Sessile Serrated Polyps Identifies Colon Cancer Subtype.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE47551
mRNA expression data from either wild-type mice or Scnn1b-transgenic mice at post-natal days 0, 3, 10, and 42
  • organism-icon Mus musculus
  • sample-icon 83 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathology associated with airway surface dehydration.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE12466
Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE47548
Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathology associated with airway surface dehydration
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; and Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84. Briefly, overexpression of the Scnn1b transgene in airway Club cells leads to hyperabsorption of sodium from the airway surface liquid, dehydrated airway surface liquid and mucus, and reduced mucus clearance associated with accumulation of mucus plugs/plaques. The data provided here represents mRNA expression data from disseccted whole trachea (distal and proximal ends cut 3-4 cartliage rings below the larynx and just above the bifurcation, respectively) from male WT and Scnn1b-Tg littermates (C57Bl/6NTac background) at 4 time points [postnatal days (PND) 0, 3, 10, and 42]. PND 0 trachea are histologically normal, a tracheal mucus plug/obstruction develops around PND 3, the plug is receding to more distal airways by PND 10, and the trachea is again histologically normal by PND 42. The data from the WT mice provides a global look at mRNA changes across time, while the data from the Scnn1b-Tg line provides mRNA data that allows differential gene expression due to mucus obstruction to be queried.

Publication Title

Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathology associated with airway surface dehydration.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE10592
Differential gene expression from azithromycin and SMM treated human airway epithelium
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarrays were used to evaluate the effects of azithromycin and an inflammatory stimulus (SMM) on human airway epithelium. Effects of azithromycin treatment were evaluated at 6, 24 and 48 hours. Effects of SMM were evaluated at 6 and 24 hours. In addition, pretreatment with azithromycin was used to evaluate the modulatory effects on SMM-induced inflammation. SMM=supernatant from microcorpulent material from human cystic fibrosis airways.

Publication Title

Azithromycin treatment alters gene expression in inflammatory, lipid metabolism, and cell cycle pathways in well-differentiated human airway epithelia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE47550
mRNA expression data from whole trachea dissected from either wild-type mice or Scnn1b-Tg mice at post-natal days 0, 3, 10, and 42
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84; and Livraghi-Butrico et al. 2012, Mucosal Immunology 5(4):397-408). Briefly, overexpression of the Scnn1b transgene in airway Club cells leads to hyperabsorption of sodium from the airway surface liquid, which causes airway surface liquid and mucus dehydration, resulting in reduced mucus clearance and airway mucus obstruction. The data provided here represents mRNA expression data from dissected whole trachea (distal and proximal ends were cut 3-4 cartilage rings below the larynx and just above the bifurcation, respectively) from male WT and Scnn1b-Tg littermates (C57Bl/6N Tac background) at 4 time points [postnatal days (PND) 0, 3, 10, and 42]. Histologically, PND 0 trachea are normal, a tracheal mucus plug/obstruction develops around PND 3 and typically recedes to the intrapulmonary airways after PND 10, and the trachea is again histologically normal by PND 42. The data from the WT mice provides a global look at mRNA post-natal developmental changes, while the data from the Scnn1b-Tg line provides mRNA data that allows differential gene expression due to airway mucus obstruction to be queried.

Publication Title

Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathology associated with airway surface dehydration.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE47546
Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathology associated with airway surface dehydration [left lobe only]
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84; and Livraghi-Butrico et al. 2012, Mucosal Immunology 5(4):397-408). Briefly, overexpression of the Scnn1b transgene in airway Club cells leads to hyperabsorption of sodium from the airway surface liquid, which causes airway surface liquid and mucus dehydration, resulting in reduced mucus clearance and airway mucus obstruction. The data provided here represents mRNA expression data from disseccted whole lung from male WT and Scnn1b-transgenic littermates (C57Bl/6NTac background) at 4 time points [postnatal days (PND) 0, 3, 10, and 42]. Histologically, PND 0 lungs are normal, at PND 3 the intrapulmonary airways exhibit transient and spotty Club cell necrosis, and by PND 10 airway mucus obstruction is evident in the proximal portion of the intrapulmonary main stem bronchus. At PND 42, Scnn1b-Tg lungs are charactyerized by chronic low level inflammation, with activated macrophages, neutrophilia, eosinophilia and increased incidence of bronchus-associated lymphoid tissue. The data from the WT mice provides a global look at mRNA post-natal developmental changes, while the data from the Scnn1b-transgenic line allows differential gene expression due to airway surface liquid dehydration and mucus obstruction to be queried.

Publication Title

Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathology associated with airway surface dehydration.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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