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Homo sapiens
36 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We integrated three transplant rejection microarray studies examining gene expression in samples from pediatric renal, adult renal, and adult heart transplants. We performed one study ourselves and retrieved two others from the NCBI Gene Expression Omnibus (GEO)(GSE4470 and GSE1563). We identified 45 genes that were upregulated in common in acute rejection. Half were involved in one immune-related pathway. Among ten proteins we tested by serum ELISA, three successfully distinguished acute rejection from stable transplants. These were CXCL9, PECAM1, and CD44, with areas under the receiver operating characteristic curves of 0.844, 0.802, and 0.738, respectively. Immunohistochemistry showed that the PECAM1 protein was increased in acute rejection in renal, liver and heart transplants versus normal tissues. Our results show that integrating publicly-available gene expression data sets is a fast, powerful, and cost-effective way to identify serum-detectable diagnostic biomarkers.
Publication Title
Integrative urinary peptidomics in renal transplantation identifies biomarkers for acute rejection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 119 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
CONTEXT Slowly progressive chronic tubulo-interstitial damage jeopardizes long-term renal allograft survival. Both immune and non-immune mechanisms are thought to contribute, but the most promising targets for timely intervention have not been identified. OBJECTIVE In the current study we seek to determine the driving force behind progressive histological damage of renal allografts, without the interference of donor pathology, delayed graft function and acute graft rejection. DESIGN We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. PATIENTS Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection. RESULTS In this highly cross-validated study, we demonstrate the significant association of established, ongoing and future chronic histological damage with regulation of adaptive immune gene expression (T-cell and B-cell transcript sets) and innate immune response gene expression (dendritic cell, NK-cell, mast cell and granulocyte transcripts). We demonstrate the ability of gene expression analysis to perform as a quantitative marker for ongoing inflammation with a wide dynamic range: from subtle subhistological inflammation prior to development of chronic damage, over moderate subclinical inflammation associated with chronic histological damage, to marked inflammation of Banff-grade acute T-cell mediated rejection. CONCLUSION Progressive chronic histological damage after kidney transplantation is associated with significant regulation of both innate and adaptive immune responses, months before the histological lesions appear. This study therefore corroborates the hypothesis that quantitative inflammation below the diagnostic threshold of classic T-cell or antibody-mediated rejection is associated with early subclinical stages of progressive renal allograft damage.
Publication Title
Progressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 166 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Polyoma virus nephropathy (PVAN) is a common cause of kidney allograft dysfunction and loss. Microscopic descriptions of PVAN are very similar to T-cell mediated rejection (TCMR) and have unclear underlying molecular mechanisms. To identify PVAN-specific gene expression, we analyzed 162 kidney biopsies with and without PVAN for global gene expression. Unsupervised hierarchical clustering analysis of all 162 biopsies revealed high similarity between PVAN and TCMR gene expression. Increasing the stringency for the specificity (p <0.001 and >2-fold expression) between PVAN and TCMR, 158 and 252 unique PVAN and TCMR injury-specific probesets were observed, respectively. While TCMR-specific probeset were overwhelmingly involved in immune response costimulation (CTLA4, CD28, CD86) and TCR (NFATC2, LCP2) signaling, PVAN-specific probesets were mainly related to viral replication process (IFITM1, LTF, NOSIP, RARRES3), RNA polymerase assembly (POLR2l, TAF10, RPS15) and pathogen recognition receptors (C1QA, C3, CFD). A principal component analysis using these genes further confirmed the most optimal separation between the 3 different clinical phenotypes. Validation of 4 PVAN-specific probesets (RPS15, CFD, LTF, and NOSIP) by QPCR and further confirmation by IHC of 2 PVAN-specific proteins with anti-viral function (LTF and IFITM1) was done, showing significantly higher expression within interstitial cellular infiltrates and in tubuli in PVAN specimens as compared to TCMR and NL kidney biopsies. In conclusion, even though PVAN and TCMR kidney allografts share great similarities on gene perturbation, particular PVAN-specific transcripts were identified with well-known anti-viral properties that provide tools for discerning PVAN and AR as well as attractive targets for rational drug design.
Publication Title
Intragraft Antiviral-Specific Gene Expression as a Distinctive Transcriptional Signature for Studies in Polyomavirus-Associated Nephropathy.
Sample Metadata Fields
Specimen part, Disease
View Samples- Escherichia coli
- 6 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
DNA microarrays were conducted on E. coli K12 cells stressed with 10 M in N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). Overall, 260 genes varied in expression, 114 up-regulated and 146 down-regulated by Zn deprivation
Publication Title
Characterization of Zn(II)-responsive ribosomal proteins YkgM and L31 in E. coli.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 88 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The biopsy samples obtained at implantation segregated in 2 distinct groups according to donor origin, with a cluster of 319 unique identified genes higher expressed in DD compared to LD kidneys, and 329 genes lower expressed (false discovery rate <5%). Using pathway analysis software a significant local renal overrepresentation of complement genes in DD implantation biopsies was identified. Complement gene expression in DD kidneys related both to donor death and cold ischemia duration, and was associated with a slower onset of renal allograft function. In post-transplantation protocol biopsies, there was a continued overexpression of complement genes, regardless of donor source. The local renal complement gene expression variability in post-transplantation biopsies correlated with renal graft function.
Publication Title
Expression of complement components differs between kidney allografts from living and deceased donors.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 76 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Gene expression data was analyzed to map with urine proteomics data
Publication Title
Mining the human urine proteome for monitoring renal transplant injury.
Sample Metadata Fields
Specimen part
View Samples
GSE14067- Homo sapiens
- 72 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In this study, we examined transcriptional profiles from 3 different microarray platforms, across 103 peripheral blood samples with and without acute rejection, to find a critical gene-set for the diagnosis of acute renal rejection that matched biopsy diagnosis, irrespective of patient demographics, clinical confounders, concomitant infection, immunosuppression usage or sample processing methods. We hypothesized that changes in peripheral blood expression profiles correlate with biopsy-proven rejection, and that these changes could be used as biomarkers for the diagnosis and prediction of acute rejection.
Publication Title
A peripheral blood diagnostic test for acute rejection in renal transplantation.
Sample Metadata Fields
Disease, Disease stage
View Samples- Homo sapiens
- 72 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In this study, we examined transcriptional profiles from 3 different microarray platforms, across 103 peripheral blood samples with and without acute rejection, to find a critical gene-set for the diagnosis of acute renal rejection that matched biopsy diagnosis, irrespective of patient demographics, clinical confounders, concomitant infection, immunosuppression usage or sample processing methods. We hypothesized that changes in peripheral blood expression profiles correlate with biopsy-proven rejection, and that these changes could be used as biomarkers for the diagnosis and prediction of acute rejection.
Publication Title
A peripheral blood diagnostic test for acute rejection in renal transplantation.
Sample Metadata Fields
Disease, Disease stage
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
An investigation of the global gene expression signatures of murine hematopoietic stem cell differentiation during steady state hematopoiesis.
Publication Title
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.
Sample Metadata Fields
Specimen part
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