Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses, suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However, a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia. We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus.
Systems-level comparison of host responses induced by pandemic and seasonal influenza A H1N1 viruses in primary human type I-like alveolar epithelial cells in vitro.
Specimen part, Subject, Time
View SamplesPrevious studies have reported that the tumour cells of nasopharyngeal carcinoma (NPC) exhibit both recurrent chromosome abnormalities and changes in the expression of numerous genes. However, it is not known to what extent changes in the copy number of individual genes are associated with the observed expression changes. To address this, a genome wide analysis of chromosome copy number and gene expression was performed in tumour cells micro-dissected from the same NPC biopsies. Significant gene expression changes were identified in tumour suppressor genes (TSGs) and in tumour-promoting genes (TPGs) but almost 60% of these can be either upregulated or downregulated in different types of cancer. This suggests that the simplistic classification of genes as TSGs or TPGs may not be entirely appropriate and that the concept of onco-suppressors may be more extensive than previously recognised. Several genomic regions showing frequent copy number gain or loss were identified. Whereas TSGs were significantly enriched within regions of frequent loss, no significant enrichment of TPGs was observed in regions of frequent gain. However, on a gene by gene basis little correlation was found between DNA copy number and alterations in gene expression except for loss of expression from homozygous deletions and a single highly amplified segment which showed enhanced gene expression.
A global view of the oncogenic landscape in nasopharyngeal carcinoma: an integrated analysis at the genetic and expression levels.
Disease, Disease stage
View SamplesIgA nephropathy (IgAN) is the most common glomerulonephritis in the world. The disease is characterized by galactose deficient IgA (gd-IgA) in the circulation forming immune complexes. The complexes are deposited in the glomerular mesangium leading to inflammation and loss of renal function, but the pathophysiology of the disease is still not fully understood. Using an integrated global transcriptomic and proteomic profiling approach we investigated the role of the mesangium in the onset and progression of IgAN. Global gene expression was investigated by microarray analysis of the glomerular compartment of renal biopsies from patients with IgAN. The influence of galactose deficient IgA (gd-IgA) on mesangial cells was investigated by proteomic profiling. By utilizing the previous published literature curated glomerular cell type-specific genes, we found that mesangial cells and their positive standard genes play a more dominant role in IgAN comparing to the podocyte standard genes. Additionally, the patient clinical parameters (serum creatinine values and estimated glomerular filtration rate - eGFR) significantly correlate with z-scores derived from expression profile of mesangial cell positive standard genes. 22 common pathways were identified both from in vivo microarray data and in vitro mesangial cell mass spectrometry data and the main part was inflammatory pathways. The correlation between clinical data and mesangial standard genes allows for a better understanding of the onset of IgAN. The genes, proteins and their corresponding pathways identified in this paper give us novel insights into the pathophysiological mechanisms leading to progression of IgAN.
Transcriptomic and Proteomic Profiling Provides Insight into Mesangial Cell Function in IgA Nephropathy.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Specimen part, Disease stage, Cell line, Subject
View SamplesMatrix induced effects on gene expression in HeLa and MDA-MB-231 cells
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Cell line
View Samplesgene expression data from 3 pairs of cancer associated fibroblasts and normal fibroblasts from the same individual Overall design: mRNA seq data from 3 normal and 3 cancer associated fibroblast cell lines
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Specimen part, Disease stage, Subject
View Samples