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accession-icon GSE36223
Molecular defense mechanisms of Barrett's metaplasia estimated by an integrative genomics
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Barrett's esophagus is characterized by the replacement of squamous epithelium with specialized intestinal metaplastic mucosa. The exact mechanisms of initiation and development of Barrett's metaplasia remain unknown, but a hypothesis of successful adaptation against noxious reflux components has been proposed. To search for the repertoire of adaptation mechanisms of Barrett's metaplasia, we employed high-throughput functional genomic and proteomic methods that defined the molecular background of metaplastic mucosa resistance to reflux. Transcriptional profiling was established for 23 pairs of esophageal squamous epithelium and Barrett's metaplasia tissue samples using Affymetrix U133A 2.0 GeneChips and validated by quantitative real-time polymerase chain reaction. Differences in protein composition were assessed by electrophoretic and mass-spectrometry-based methods. Among 2,822 genes differentially expressed between Barrett's metaplasia and squamous epithelium, we observed significantly overexpressed metaplastic mucosa genes that encode cytokines and growth factors, constituents of extracellular matrix, basement membrane and tight junctions, and proteins involved in prostaglandin and phosphoinositol metabolism, nitric oxide production, and bioenergetics. Their expression likely reflects defense and repair responses of metaplastic mucosa, whereas overexpression of genes encoding heat shock proteins and several protein kinases in squamous epithelium may reflect lower resistance of normal esophageal epithelium than Barrett's metaplasia to reflux components. Despite the methodological and interpretative difficulties in data analyses discussed in this paper, our studies confirm that Barrett's metaplasia may be regarded as a specific microevolution allowing for accumulation of mucosal morphological and physiological changes that better protect against reflux injury.

Publication Title

Molecular defense mechanisms of Barrett's metaplasia estimated by an integrative genomics.

Sample Metadata Fields

Sex, Age

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accession-icon GSE28244
Expression profile of maizes stalk challenged with the corn borer Sesamia nonagrioides
  • organism-icon Zea mays
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Stalk borers are major pests for some of the most important crops in the world, such as maize or rice. Plant defense mechanisms against these herbivores have been poorly investigated. The maizes stalk responds to insect feeding activating defense genes including hormone biosynthetic-related or proteinase inhibitor transcripts. The most outstanding conclusion is that cells in the maizes stalk undergo cell wall fortification after corn borer tunneling.

Publication Title

Inducible maize defense mechanisms against the corn borer Sesamia nonagrioides: a transcriptome and biochemical approach.

Sample Metadata Fields

Specimen part

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accession-icon SRP125292
Transciptomic analysis of maize response to the attack of Sesamia nonagrioides
  • organism-icon Zea mays
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We performed a transcriptomic analysis to identify genes differentially transcribed in the maize stem upon corn borer feeding and treatment with insects regurgitates by using the MACE (Massive Analysis of cDNA Ends) technology. Overall design: Two comparisons were performed: Insect chewing vs control and Regurgitate+wounding vs wounding in three biological replicates per treatment

Publication Title

Maize Stem Response to Long-Term Attack by <i>Sesamia nonagrioides</i>.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE41956
Transcriptome analysis of A661 leaves
  • organism-icon Zea mays
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

The maize inbred line A661 shows a characteristic phenotype when grown at suboptimal temperatures for three weeks and then is exposed to optimal temperatures for one extra week. After this period the third leaf showed two well defined sections: distal (chlorophyll-less; CL) and proximal (chlorophyll-containing; CC) sections. To further investigate the performance of the inbred line A661 under cold conditions a gene expression profiling analysis was conducted using large scale maize microarrays. A total of 1002 transcripts change their expression between both leaf sections and the majority of these codify for proteins located to the chloroplast.

Publication Title

Genetic regulation of cold-induced albinism in the maize inbred line A661.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49116
Protective Role of IL6 in Vascular Remodeling in Schistosoma-Pulmonary Hypertension
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE48936
Murine Schistosoma-Induced Pulmonary Hypertension: Microarray Data
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Rationale: Schistosomiasis is one of the most common causes of pulmonary arterial hypertension worldwide, but the pathogenic mechanism by which the host inflammatory response contributes to vascular remodeling is unknown. We sought to identify signaling pathways that play protective or pathogenic roles in experimental Schistosoma-induced pulmonary vascular disease by whole-lung transcriptome analysis. Methods: Wildtype mice were experimentally exposed to S. mansoni ova by intraperitoneal sensitization followed by tail vein augmentation, and the phenotype assessed by right ventricular catheterization and tissue histology, RNA and protein analysis. Whole-lung transcriptome analysis by microarray and RNA sequencing was performed, the latter analyzed using 2 bioinformatic methods. Functional testing of the candidate IL-6 pathway was determined using IL6-knockout mice and the STAT3 inhibitor STI-201. Results: Wild-type mice exposed to S. mansoni had increased right ventricular systolic pressure and thickness of the pulmonary vascular media. Whole lung transcriptome analysis identified the IL6-STAT3-NFATc2 pathway as being upregulated, which was confirmed by PCR and immunostaining of lung tissue from S. mansoni-exposed mice and patients who died of the disease. Mice lacking IL6 or treated with STI-201 developed pulmonary hypertension associated with significant intima remodeling after exposure to S. mansoni. Conclusions: Whole lung transcriptome analysis identified upregulation of the IL6-STAT3-NFATc2 pathway, and IL6 signaling was found to be protective against Schistosoma-induced intimal remodeling.

Publication Title

Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, 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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