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accession-icon SRP055930
Alteration in the transcriptome of the lung during TGFa-induced pulmonary fibrosis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Pulmonary fibrosis (PF) is associated with many chronic lung diseases including Systemic sclerosis (SSc), Idiopathic Pulmonary Fibrosis (IPF) and Cystic Fibrosis (CF) which are characterized by the progressive accumulation of stromal cells and formation of scar tissue. Pulmonary fibrosis is a dysregulated response to alveolar injury which causes a progressive decline in lung function and refractory to current pharmacological therapies. Airway and alveolar epithelial cells and stromal cells contribute to pulmonary fibrosis but the cell-specific pathways and gene networks that are responsible for the pathophysiology are unknown. Recent animals models generated in our lab demonstrate clinical phenotypes seen in human fibrotic disease. The mouse model of transforming growth factor-a (TGFa)-induced fibrosis include conditionally expressing TGFa in the lung epithelium under control of the CCSP promoter driving rtTA expression (CCSP/TGFa). This allow the TGFa is only expressed in airway and alveolar epithelial cells and only when mice fed doxycycline (Dox). Similar to PF in humans, TGFa mice on Dox developed a progressive and extensive adventitial, interstitial and pleural fibrosis with a decline in lung mechanics. Thus, the TGFa transgenic mouse is a powerful model to determine lung cell-specific molecular signatures involved in pulmonary fibrosis. In this study, we sought to determine changes in the transcriptome during TGFa-induced pulmonary fibrosis. Our results showed that several pro-fibrotic genes increased in the lungs of TGFa mice. This study demonstrates that WT1 network gene changes associated with fibrosis and myfibroblast accumulation and thus may serve as a critical regulator fibrotic lung disease. Overall design: mRNA profiles of CCSP/- and CCSP/TGFalpha mice treated with Dox

Publication Title

Fibrocytes Regulate Wilms Tumor 1-Positive Cell Accumulation in Severe Fibrotic Lung Disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064004
Transplantation of gastric organoid-derived spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) cell lineage promotes ulcer repair in the aged stomach
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Background & Aims: Spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) is known to emerge following parietal cell loss and during Helicobacter pylori infection, however its role in gastric ulcer repair is unknown. Therefore, we sought to investigate if SPEM plays a role in epithelial regeneration. Methods: Acetic acid ulcers were induced in young (2-3 months) C57BL/6 mice to determine the quality of ulcer repair. Gastric tissue was collected and analyzed to determine the expression of SPEM within the regenerating epithelium. As a comparison to native tissue the expression of SPEM was also identified within cultured gastric mouse-derived organoids. Results: Wound healing in the mice coincided with the emergence of SPEM expressing CD44v within the ulcerated region. The emergence of SPEM was also observed in cultured gastric organoids. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. Overall design: 4 samples were used for ulcerated and uninjured tissue. 1 sample was used for intact tissue and organoid-derived RNA. The 'Ulcerated' samples represent C57BL/6 mice with ulcers and the 'Uninjured' samples represent the healthy controls (for "ulcerated" samples). The "Intact stomach tissue" and "Gastric organoids" samples are other types of samples that compared separately. "Gastric organoids" in this comparison are derived from "Intact stomach tissue".

Publication Title

The Development of Spasmolytic Polypeptide/TFF2-Expressing Metaplasia (SPEM) During Gastric Repair Is Absent in the Aged Stomach.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE15182
Comparison of ATG5-/- Bcl-2 tumors expressing p62-GFP versus those expressing EGFP
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Autophagy is a starvation response that facilitates cell survival under metabolic stress and yet defects in autophagy promote tumorigenesis. While the role of understarvation is relatively clearer, its mechanistic role in tumorigenesis is poorly understood. We show that defective autophagy promotes protein damage and accumulation of p62, a marker for protein damage accumulation that is cleared through autophagy pathway. The failure to eliminate p62 in autophagy-defective cells, leads to deregulation of cell signalling and gene expression and ultimately promotes tumorigenesis. Thus defective-autophagy is a mechanism for p62 accumulation commonly observed in human tumors.

Publication Title

Autophagy suppresses tumorigenesis through elimination of p62.

Sample Metadata Fields

Cell line

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accession-icon GSE33785
Gene expression in the chronic ethanol-treated rat liver during liver regeneration
  • organism-icon Rattus norvegicus
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

In this study, we analyzed the effects of chronic alcohol consumption on liver repair and regeneration after partial hepatectomy (PHx). Rats were fed a liquid diet containing 36% of total calories derived from ethanol for 5 weeks; corresponding pair-fed calorie-matched controls were fed diets in which ethanol calories were replaced either by carbohydrate or by fat. After 5 weeks, rats were subjected to 70% PHx and liver samples were collected at 1, 6 and 24h after the surgery. The excised liver samples at t=0 served as within-animal controls. We used Affymetrix Rat Gene 1.0 ST arrays to obtain global gene expression data from each liver sample (n=4 replicate rats, 72 arrays total).

Publication Title

Chronic ethanol feeding enhances miR-21 induction during liver regeneration while inhibiting proliferation in rats.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE23006
Transcriptional profiling of a wound healing process in skin and oral mucosa
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

When compared to skin, oral mucosal wounds heal rapidly and with reduced scar formation. This study used an Affymetrix microarray platform to compare the transcriptomes of oral mucosa and skin wounds in order to identify critical differences in the healing response at these two sites.

Publication Title

Positional differences in the wound transcriptome of skin and oral mucosa.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE67242
Analysis of the role of miR-21 in liver regeneration after partial hepatectomy (PHx) in chronic ethanol-treated rats through in vivo inhibition using LNAs
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

In this study, we analyzed the role of miR-21 in liver regeneration after partial hepatectomy (PHx) in chronic ethanol-treated rats. Male Sprague-Dawley rats were fed a liquid diet containing 36% of total calories derived from ethanol for 5 weeks; corresponding pair-fed calorie-matched controls were fed diets in which ethanol calories were replaced by carbohydrate. After 5 weeks, locked nucleic acid (LNA)-modified oligo antisense to miR-21 (AM21, Exiqon, Vedbaek, Denmark) was used to inhibit miRNA in vivo, and rats were subjected to 70% PHx. Liver samples were collected at 24h after the surgery. The excised liver samples at t=0 served as within-animal controls. Rat Gene 2.0 ST (Affymetrix, Santa Clara, CA) arrayswere used to obtain global gene expression data from pooled liver samples (pools of 3 or 4 biological replicates/array, total 8 arrays).

Publication Title

Inhibition of miR-21 rescues liver regeneration after partial hepatectomy in ethanol-fed rats.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE12748
Weighted Gene Coexpression Network Analysis Identifies Biomarkers in Glycerol Kinase Deficient Mice
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Symptomatic glycerol kinase deficiency (GKD) is associated with episodic metabolic and central nervous system deterioration. We report here the first application of Weighted Gene Co-Expression Network Analysis (WGCNA) to investigate a knockout (KO) murine model of a human genetic disease. WGCNA identified networks and key hub transcripts from liver mRNA of glycerol kinase (Gyk) KO and wild type (WT) mice. Day of life 1 (dol1) samples from KO mice contained a network module enriched for organic acid metabolism before Gyk KO mice develop organic acidemia and die on dol3-4 and the module containing Gyk was enriched with apoptotic genes. Roles for the highly connected Acot, Psat and Plk3 transcripts were confirmed in cell cultures and subsequently validated by causality testing. We provide evidence that GK may have an apoptotic moonlighting role that is lost in GKD. This systems biology strategy has improved our understanding of GKD pathogenesis and suggests possible treatments.

Publication Title

Weighted gene co-expression network analysis identifies biomarkers in glycerol kinase deficient mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE95012
Loss of Cic leads to aberrant neural stem cell proliferation and differentiation and promotes gliomagenesis
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Mouse neural stem cells were generated from conditional knockout mice (Cicflox/flox) or the wild trype control mice (Cic+/+). Cic is conditionally knocked out following expression of Cre-recombinase. Cre-recombinase was incorporated in vitro via adenoviral-Cre transduction.

Publication Title

<i>Cic</i> Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE2665
Lymphe node vs. Tonsil
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Lymph node vs. tonsil

Publication Title

Differential expression of a gene signature for scavenger/lectin receptors by endothelial cells and macrophages in human lymph node sinuses, the primary sites of regional metastasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP014006
RNA sequencing in fly heads to examine the effect of spermidine feeding on transcription in the ageing fly brain.
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx, Illumina HiSeq 2000

Description

mRNA sequencing was used to identify genome wide transcriptional changes occuring in fly heads in response to spermidine feeding. This study shed light on the molecular mechanisms through wich spermidine can protect against age-dependent memory impairment. Overall design: mRNA profiles from 3 and 10 day old Drosophila melanogaster heads were generated in duplicate by deep sequencing using Illumina GAIIx. mRNA profiles from flies that were fed food with 5mM spermidine were compared to profiles from flies that had no spermidine in thier food.

Publication Title

Restoring polyamines protects from age-induced memory impairment in an autophagy-dependent manner.

Sample Metadata Fields

Age, Specimen part, 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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