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accession-icon GSE29285
C/EBPa Regulates Protease/anti-protease Balance and Mediates Bronchiolar Cell Recovery After Injury
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In the present study, we hypothesized that C/EBPa (CCAAT/enhancer-binding protein alpha) plays a role in cell regeneration in response to bronchiolar epithelial cell injury. C/EBPa mediated ciliated cell regeneration after naphthalene bronchiolar epithelial cell injury in vivo. Furthermore, we demonstrated that C/EBPa regulates protease/anti-protease balance after lung injury, and intratracheal treatment with anti-protease (BPTI) restored ciliated cell regeneration after naphthalene injury in CebpaD/D mice.

Publication Title

CCAAT/enhancer binding protein-α regulates the protease/antiprotease balance required for bronchiolar epithelium regeneration.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE6846
Gene Expression and Biological Processes Influenced By Deletion of Stat3 in pulmonary Alveolar Type II Cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Deletion of Stat3 induced genes influencing protein metabolism, transport, chemotaxis and apoptosis and decreased the expression of genes mediating lipid synthesis and metabolism. Srebf1 and 2, key regulators of fatty acid and steroid biosynthesis, were decreased in Stat3D/D mice. Stat3 influenced both pro- and anti-apoptotic pathways, regulating and maintaining the balance between a subset of pro- and anti-apoptotic genes that determine cell death or survival. Akt, a known target of Stat3, participates in many Stat3 mediated pathways including Jak-Stat signaling, apoptosis, the MAPK signaling, cholesterol and fatty acid biosynthesis. Deletion of Stat3 from type II epithelial cells altered the expression of genes regulating diverse cellular processes, including cell growth and apoptosis, lipid biosynthesis and metabolism. Stat3 regulates cell formation through a complex regulatory network that likely enhances alveolar epithelial cell survival and surfactant/lipid synthesis, necessary for the protection of the lung during injury.

Publication Title

Gene expression and biological processes influenced by deletion of Stat3 in pulmonary type II epithelial cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14917
C/EBPa is required for pulmonary cytoprotection from hyperoxia injury
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We have previously demonstrated that deletion of the Cebpa gene in the developing fetal mouse lung caused death soon after birth from the failure of lung maturation. Many of the transcriptional pathways regulating morphogenesis of the fetal lung are induced postnatally and mediate repair of the injured lung. We hypothesized that C/EBPa plays a role in protection of the alveolar epithelium following hyperoxia injury of the mature lung. Transgenic Cebpa/ mice in which Cebpa was conditionally deleted from Clara cells (from early gestation) and type II cells (from near-term) were developed. Cebpa/ mice grow normally without any pulmonary abnormalities. Cebpa/ mice were highly susceptible to hyperoxia. Cebpa/ mice died within 4d after hyperoxia associated with severe lung inflammation and altered surfactant components at a time when all control mice survived. Microarrays were analyzed on isolated type II cells at an early stage (24h) of hyperoxia exposure to detect the primary genes influenced by deletion of Cebpa. The associated network analysis revealed the reduced expression of key genes related to surfactant lipid and protein homeostasis, such as Srebf, Scap, Lpcat1, Abca3, Sftpb, and Napsa. Genes for the cell signaling, immune response, and protective antioxidants, including GSH and Vnn-1,3, were decreased in the Cebpa/ mice lung. C/EBPa did not play a critical role in postnatal pulmonary function under normal conditions. In contrast, in the absence of C/EBPa, exposure to hyperoxia caused respiratory failure, supporting the concept that C/EBPa plays an important role in enhancing epithelial cell survival, surfactant lipid homeostasis, and maturation of SP-B from pro-SP-B.

Publication Title

C/EBP{alpha} is required for pulmonary cytoprotection during hyperoxia.

Sample Metadata Fields

Specimen part

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accession-icon GSE45487
Identification of genes responsive to low-intensity pulsed ultrasound (LIPUS) in MC3T3-E1 preosteoblast cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Although LIPUS has been shown to enhance fracture healing, the underlying mechanism of LIPUS remains to be fully elucidated. Here, to understand the molecular mechanism underlying cellular responses to LIPUS, we investigated gene expression profiles in mouse MC3T3-E1 preosteoblast cells using a GeneChip system.

Publication Title

Genes responsive to low-intensity pulsed ultrasound in MC3T3-E1 preosteoblast cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

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accession-icon GSE19679
The influence of Snail expression on mRNA transcription levels in II-18 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Snail is a transcriptional repressor, which induces epithelial-mesenchymal transition. However, overall functions of Snail remain to be elucidated. This microarray was performed to investigate the influence of Snail expression on mRNA transcription levels in a lung adenocarcinoma cell line, II-18.

Publication Title

Epithelial-mesenchymal transition abolishes the susceptibility of polarized epithelial cell lines to measles virus.

Sample Metadata Fields

Cell line

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accession-icon GSE53397
The expression profiling comparison of mice with Scap and Insig deletion from perinatal lung (E17.5-PN1)
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In this study, we studied the genomic responses of the Insig and Scap deletion from perinatal lung.

Publication Title

Epithelial SCAP/INSIG/SREBP signaling regulates multiple biological processes during perinatal lung maturation.

Sample Metadata Fields

Specimen part

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accession-icon GSE31797
Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: Lung function is dependent upon the precise regulation of the synthesis, storage, and catabolism of tissue and alveolar lipids.

Publication Title

Activation of sterol-response element-binding proteins (SREBP) in alveolar type II cells enhances lipogenesis causing pulmonary lipotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE35485
Transcriptional Programs Controlling Perinatal Lung Maturation
  • organism-icon Mus musculus
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In this study, time dependent genome wide lung mRNA profiling changes were assessed using C57BL/6J and A/J mice. Through comprehensive bioinformatics and functional genomics analyses, we identified both temporal and strain dependent gene expression patterns, systemically mapped key regulators, bioprocesses, and transcriptional networks controlling lung maturation, providing the basis for new therapeutic strategies to enhance lung function in preterm infants.

Publication Title

Transcriptional programs controlling perinatal lung maturation.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE9743
The in vivo effect of actin cytoskeletal abnormalities on gene expression
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Remodeling of the actin cytoskeleton through actin dynamics (assembly and disassembly of filamentous actin) is known to be essential for numerous basic biological processes. In addition, recent in vitro studies provided evidence that actin dynamics participate in the control of gene expression. A spontaneous mouse mutant, corneal disease 1 (corn1), is deficient for a regulator of actin dynamics, destrin (DSTN; also known as actin depolymerizing factor or ADF), and develops epithelial hyperproliferation and neovascularization in the cornea. Dstncorn1 mice exhibit the actin dynamics defect in the corneal epithelial cells as evidenced by increased filamentous actin, offering an in vivo model to investigate the physiological significance of the transcriptional regulation by actin dynamics. To examine the effect of the Dstncorn1 mutation on gene expression, we performed a microarray analysis using the cornea from Dstncorn1 and wild-type control mice. A dramatic alteration of gene expression was observed in the Dstncorn1 cornea, with 1,226 annotated genes differentially expressed. Functional annotation of these genes revealed that most significantly enriched functional categories are associated with actin and/or cytoskeleton. Among genes that belong to these categories, a considerable number of serum response factor (SRF) target genes were found, indicating the existence of the actin-SRF pathway of transcriptional regulation in vivo. A comparative study using an allelic mutant strain, Dstncorn1-2J, with milder corneal phenotypes also suggested that the severity of the actin dynamics defect correlates with the level of gene expression changes. Our study provides evidence that actin dynamics have a strong impact on gene expression in vivo.

Publication Title

Effect of destrin mutations on the gene expression profile in vivo.

Sample Metadata Fields

Sex, Age

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accession-icon GSE49486
Effect of ingested whey protein hydrolysate on gene expression profiles compared to an identical composition of amino acid mixture in rat skeletal muscle
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

We have previously showed that whey protein hydrolysate (WPH) causes a greater increase in muscle protein synthesis than an identical composition of amino acids mixture does. The present study was conducted to investigate a comparative effect of WPH on gene expression. Male Sprague-Dawley rats subjected to a 2-h swimming exercise were administered either a carbohydrate-amino acid diet or a carbohydrate-WPH diet immediately after exercise. One hour after exercise, epitrochlearis muscle mRNA was sampled and subjected to DNA microarray analysis. As a result, ingestion of WPH altered 189 genes in considering the false discovery rate. Among the upregulated genes, 8 Gene Ontology (GO) terms were enriched, which included key elements in muscle repair after exercise such as Cd24, Ccl2, Ccl7 and Cxcl1. On the other hand, 9 GO terms were enriched in the gene sets downregulated by ingestion of WPH and these GO terms fell into 2 clusters, regulation of ATPase activity, and immune response. Furthermore, we found that WPH activate the 2 upstream proteins, extracellular signal-regulated kinase 1/2 (ERK1/2) and hypoxia-inducible factor-1 (HIF-1), which may act as key factors for regulation of gene expression. These results suggest that ingestion of WPH, compared to an identical composition of amino acid mixture, induces greater changes in the after-exercise gene expression profile via activation of the proteins, ERK1/2 and HIF-1.

Publication Title

Post-exercise impact of ingested whey protein hydrolysate on gene expression profiles in rat skeletal muscle: activation of extracellular signal-regulated kinase 1/2 and hypoxia-inducible factor-1α.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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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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