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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Glomeruli vs. Control Glomeruli)

ABSTRACT: We 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. Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. Stringent statistical analysis using the Benjamini_Hochberg corrected 2-tailed t-test was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. This Series includes DKD and control glomeruli samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Karolina Woroniecka

PROVIDER: E-GEOD-30528 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptome analysis of human diabetic kidney disease.

Woroniecka Karolina I KI Park Ae Seo Deok AS Mohtat Davoud D Thomas David B DB Pullman James M JM Susztak Katalin K

Diabetes 20110713 9

<h4>Objective</h4>Diabetic kidney disease (DKD) is the single leading cause of kidney failure in the U.S., for which a cure has not yet been found. The aim of our study was to provide an unbiased catalog of gene-expression changes in human diabetic kidney biopsy samples.<h4>Research design and methods</h4>Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. DKD samples were significant for their racial diversity and de ...[more]

PMID: 21752957

Similar Datasets

Transcriptome Analysis of Human Diabetic Kidney Disease (Control Glomeruli vs. Control Tubuli)

Project description:We 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. Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. Stringent statistical analysis using the Benjamini_Hochberg corrected 2-tailed t-test was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. This Series includes control glomeruli and tubuli samples.

2011-08-02 | E-GEOD-30566 | biostudies-arrayexpress

Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli)

2011-08-02 | E-GEOD-30529 | biostudies-arrayexpress

Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Glomeruli vs. Control Glomeruli)

2011-08-03 | GSE30528 | GEO

Transcriptome Analysis of Human Diabetic Kidney Disease (Control Glomeruli vs. Control Tubuli)

2011-08-03 | GSE30566 | GEO

Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli)

2011-08-03 | GSE30529 | GEO

Transcriptome Analysis of Human Diabetic Kidney Disease

Project description:This SuperSeries is composed of the following subset Series: GSE30528: Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Glomeruli vs. Control Glomeruli) GSE30529: Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli) GSE30566: Transcriptome Analysis of Human Diabetic Kidney Disease (Control Glomeruli vs. Control Tubuli) Refer to individual Series

2011-08-02 | E-GEOD-30122 | biostudies-arrayexpress

LSAGE Library Human Renal Glomeruli

Project description:Glomeruli were isolated from the kidney of a 72 yo male patient. The kidney was surgically removed due to renal cell carcinoma. The glomeruli were isolated from uninvolved renal parenchyma. Histology (H&E) of glomeruli and interstitium was normal. Keywords: Kidney Subcompartment Glomeruli were isolated using the sieving technique in ice-cold PBS, followed by isolation of total RNA with RNeasy kit. RNA was judged intact by agarose gel electrophoresis. SAGE library was custom-synthesized by Genzyme Corportation.

2007-06-12 | E-GEOD-8114 | biostudies-arrayexpress

Homo sapiens

Project description:Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli)

| PRJNA154759 | ENA

Proteomics Reveals Extracellular Matrix Injury in the Glomeruli and Tubulointerstitium of Kidney Allografts with Early Antibody-Mediated Rejection

Project description:Antibody-mediated rejection (AMR) accounts for >50% of kidney allograft losses. AMR is caused by donor-specific antibodies (DSA) against HLA and non-HLA antigens in the glomeruli and the tubulointerstitium, which together with high interferon gamma (IFNɣ) and tumor necrosis factor-alpha (TNFα), trigger graft injury. Unfortunately, the mechanisms governing cell-specific injury in AMR remain unclear. We studied 30 for-cause kidney biopsies with early AMR, acute cellular rejection or acute tubular necrosis (‘non-AMR’). We laser-captured microdissected glomeruli and tubulointerstitium and subjected them to unbiased proteome analysis. 120/2026 glomerular and 180/2399 tubulointerstitial proteins were significantly differentially expressed in AMR vs. non-AMR biopsies (p<0.05). Basement membrane and extracellular matrix (ECM) proteins were significantly decreased in both AMR compartments. We verified decreased glomerular and tubulointerstitial LAMC1 expression, and decreased glomerular NPHS1 and PTPRO expression in AMR. Cathepsin-V (CTSV) was predicted to cleave ECM-proteins in the AMR glomeruli, and CTSL, CTSS and LGMN in the tubulointerstitium. We identified galectin-1, an immunomodulatory protein upregulated in AMR glomeruli and linked to the ECM. Anti-HLA class-I antibodies significantly increased CTSV expression, and galectin-1 expression and secretion, in human glomerular endothelial cells. We also studied glutathione S-transferase omega-1 (GSTO1), an ECM-modifying enzyme, increased in the AMR tubulointerstitium. GSTO1 expression was significantly increased in TNFα-treated proximal tubular epithelial cells. IFNɣ and TNFα significantly increased CTSS and LGMN expression in these cells. Basement membranes are often remodeled in chronic AMR, and we demonstrated that this remodeling begins early in glomeruli and tubulointerstitium. Targeting ECM-remodeling in AMR may represent a new therapeutic opportunity.

2020-09-22 | PXD017580 | Pride

LSAGE Library Human Renal Glomeruli

2007-06-13 | GSE8114 | GEO

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