Examined the expression effects of supplementing Drosophila food on heart and nephrocyte complexes
Diet-Induced Podocyte Dysfunction in Drosophila and Mammals.
Sex, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptome analysis of human diabetic kidney disease.
Specimen part, Disease, Disease stage, Subject
View SamplesWe identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Transcriptome analysis of human diabetic kidney disease.
Specimen part, Disease, Disease stage, Subject
View SamplesWe identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Transcriptome analysis of human diabetic kidney disease.
Specimen part, Disease, Disease stage, Subject
View SamplesWe identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Transcriptome analysis of human diabetic kidney disease.
Specimen part, Disease, Disease stage
View SamplesNext-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived normal human kidney transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Overall design: The kidney tissue was immediately placed and stored in RNAlater® (Ambion), according to the manufacturer’s instruction. The tissue was manually microdissected under microscope in RNAlater® pool for glomerular and tubular compartment. Dissected tissue was homogenized and RNA was prepared using RNAeasy mini columns (Qiagen, Valencia, CA, US), according to the manufacturer’s instructions. RNA quality and quantity were determined using the Laboratory-on-Chip Total RNA PicoKit Agilent BioAnalyzer. Only samples without evidence of degradation were further used (RNA Integrity Number >6).
Functional genomic annotation of genetic risk loci highlights inflammation and epithelial biology networks in CKD.
No sample metadata fields
View SamplesThe association of cytosine methylation and gene expression in the human kidneys is yet to be determined, here we have 25 pairs of the methylation and gene expression profile.
Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development.
Specimen part
View SamplesTo identify RNA transcripts involved in acute and chronic renal epithelial injury, we performed unbiased whole transcriptome profiling of human proximal tubular epithelial cells (PTECs) in hypoxic and inflammatory conditions. RNA sequencing (RNA-seq) revealed that the protein-coding and noncoding transcriptomic landscape differed between hypoxia-stimulated and cytokine-stimulated human PTECs. Overall design: Examination of transcriptomic response of human PTECs to hypoxic or inflammatory injury
The long noncoding RNA landscape in hypoxic and inflammatory renal epithelial injury.
Specimen part, Treatment, Subject
View SamplesMales are 50% more likely to develop end stage kidney failure compared to women. In this study we wanted to find out the molecular mechanism responsible for this increased risk. We collected kidney samples from patients with and without kidney disease and performed a comprehensive gene expression analysis in healthy and diseased male and female kidneys.
Human and murine kidneys show gender- and species-specific gene expression differences in response to injury.
No sample metadata fields
View SamplesMales are 50% more likely to develop end stage kidney failure compared to women. As a model of the human condition we analyzed gene expression changes in healthy and diseased mouse kidneys.
Human and murine kidneys show gender- and species-specific gene expression differences in response to injury.
No sample metadata fields
View Samples