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E-GEOD-76882

ABSTRACT: Gene Expression in Biopsies of Acute Rejection and Interstitial Fibrosis/Tubular Atrophy Reveals Highly Shared Mechanisms that Correlate with Worse Long-term Outcomes

OTHER RELATED OMICS DATASETS IN: PRJNA308848

PROVIDER: E-GEOD-76882 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-76882-analysis-methods.tsv	Tabular
	E-GEOD-76882-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-76882-configuration.xml	Xml
	E-GEOD-76882-percentile-ranks.tsv	Tabular
	E-GEOD-76882.condensed-sdrf.tsv	Tabular

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Project description:Gene Expression in Biopsies of Acute Rejection and Interstitial Fibrosis/Tubular Atrophy Reveals Highly Shared Mechanisms that Correlate with Worse Long-term Outcomes

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Genomics of Chronic Rejection

Project description:We hypothesized that T cell-mediated immune mechanisms play a role in two conditions; 1: donor-specific antibody (DSA) negative transplant glomerulopathy (TGP) and 2: interstitial fibrosis and tubular atrophy (IFTA) with inflammation (i>0). We investigated gene expression profiles of those biopsies compared to biopsies with antibody-mediated rejection(ABMR) and to biopsies with non-specific IFTA and no inflammation. DSA negative TGP and IFTA with inflammation biopsies have a unique molecular signature distinct to that seen in biopsies with ABMR and IFTA without inflammation with significant expression of cytotoxic and regulatory T cells.

2017-01-17 | GSE93658 | GEO

Molecular Profiles Associated with Calcineurin Inhibitor Toxicity Post-Kidney Transplant: Input to Chronic Allograft Dysfunction

Project description:The molecular basis of calcineurin inhibitor toxicity (CNIT) in kidney transplantation (KT) and its contribution to chronic allograft dysfunction (CAD) with interstitial fibrosis (IF) and tubular atrophy (TA) were evaluated. Molecular signatures characterizing CNIT samples were identified. The recognized CNIT gene signature was most common in patients with decreased graft function and histological evidence of IF/TA. To test CNIT contribution to CAD progression, kidney biopsies from transplant recipients with histological diagnosis of CNIT (n=14), acute rejection (ACR, n=13), and CAD with IF/TA (n=10), including 18 Normal allografts, were analyzed using gene expression microarrays.

2014-06-01 | E-GEOD-53605 | biostudies-arrayexpress

The clinical and genomic significance of donor-specific antibody (DSA) positive/C4d negative and DSA negative/C4d negative transplant glomerulopathy

Project description:We investigated the clinical, histopathologic and genomic features of donor-specific antibody (DSA) +/C4d- and DSA-/C4d- transplant glomerulopathy (TGP) using microarrays. Comparison of the gene expression profiles of DSA-/C4d- TGP biopsies with ptc+g score > 1 to normal and IFTA (Interstitial Fibrosis and Tubular Atrophy) biopsies by microarrays revealed increased expression of quantitative cytotoxic T cell--associated transcripts (QCAT). However, CAMR (chronic antibody-mediated rejection) and DSA+/C4d- TGP had increased expression of QCAT, interferon-gamma and rejection induced, constitutive macrophage-associated, natural killer cell-associated, and DSA selective transcripts. B cell and endothelial cell associated transcripts expression were upregulated only in CAMR biopsies. Our results suggest that while DSA+/C4d- TGP should be classified under CAMR, DSA-/C4d- TGP with ptc+g score > 1 probably develops through a chronic cellular immune response. Total of 57 arrays included in this study. G1. Normal transplant kidney biopsies (N= 12); G2. Non-specific IFTA (N= 17); G3. TGP DSA-/C4d- (N=8); G4. TGP DSA+/C4d- (N= 9); G5. CAMR/TGP C4d+/DSA+ (N= 11)

2013-02-07 | E-GEOD-44131 | biostudies-arrayexpress

Exploring kidney allograft rejection: A proof-of-concept study using spatial transcriptomics

Project description:In this proof-of-concept study, spatial transcriptomics combined with public single-cell RNA sequencing data were used to explore the potential of this technology to study kidney allograft rejection. We aimed to map gene expression patterns within diverse pathological states by examining biopsies classified across non-rejection, T cell-mediated acute rejection, and interstitial fibrosis and tubular atrophy (IFTA). Our results revealed distinct immune cell signatures, including those of T and B lymphocytes, monocytes, mast cells, and plasma cells, and their spatial organization within the renal interstitium. We also mapped chemokine receptors and ligands to study immune-cell migration and recruitment. Finally, our analysis demonstrated differential spatial enrichment of transcription signatures associated with kidney allograft rejection across various biopsy regions. Interstitium regions displayed higher enrichment scores for rejection-associated gene expression patterns than did tubular areas, which had negative scores. This implies that these signatures are primarily driven by processes unfolding in the renal interstitium. Overall, this study highlights the value of spatial transcriptomics for revealing cellular heterogeneity and immune signatures in renal transplant biopsies, and demonstrates its potential for studying the molecular and cellular mechanisms associated with rejection. However, certain limitations must be borne in mind regarding the development and future applications of this technology.

2024-05-02 | GSE245870 | GEO

The clinical and genomic significance of donor-specific antibody (DSA) positive/C4d negative and DSA negative/C4d negative transplant glomerulopathy

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Redefining the molecular rejection states in 3230 heart transplant biopsies: relationships to parenchymal injury and graft survival

Project description:The first-generation Molecular Microscope® (MMDx) system for heart transplant endomyocardial biopsies used expression of rejection-associated transcripts (RATs) to diagnose T cell-mediated rejection (TCMR) and antibody-mediated rejection (ABMR) but also detected acute injury. However, the ideal system should detect rejection without being influenced by injury, to permit analysis of the relationship between rejection and parenchymal injury. To achieve this, we developed a new rejection classification in an expanded cohort of 3230 biopsies: 1641 from INTERHEART (ClinicalTrials.gov #NCT02670408), plus 1589 service biopsies added to improve the power of the machine learning algorithms. The new system used six rejection classifiers instead of RATs and generated seven rejection archetypes: No Rejection 48%; Minor 24%; TCMR1 2.3%; TCMR2 2.7%; TCMR/Mixed 2.7%; EABMR 3.9%; and FABMR 16%. Using rejection classifiers eliminated cross-reactions with acute injury, permitting separate assessment of rejection and injury. TCMR was associated with severe recent injury and late atrophy-fibrosis and rarely had normal parenchyma. ABMR was better tolerated, seldom producing severe injury, but in later biopsies was often associated with atrophy-fibrosis, indicating long term risk. Graft survival and LVEF were reduced in hearts with TCMR, but also in hearts with severe-recent injury and atrophy-fibrosis, even without rejection.

2024-04-02 | GSE262742 | GEO

Proteomic Analysis of Minimally Damaged Renal Tubular Tissue from Two-Kidney-One-Clip Hypertensive Rats Demonstrates Extensive Changes Compared to Tissue from Controls

Project description:Tubular atrophy and interstitial fibrosis present the final stage in most forms of progressive kidney diseases. Little is known regarding the early changes in the tubular proteome. In this study, we investigated changes in the tubular proteome of normal or near-normal tubular tissue in the non-clipped kidney from rats with two-kidney one-clip (2K1C) hypertension

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RNA-seq analysis of dickkopf-3 knockout and C57Bl/6 mice kidneys 7 days after unilateral ureteral obstruction

Project description:Renal tubular atrophy and interstitial fibrosis are common hallmarks of etiologically different progressive chronic kidney diseases (CKD) that eventually result in organ failure. We identify Dickkopf-3 (Dkk3) as a stress-induced, tubular epithelia-derived mediator of kidney fibrosis. Genetic as well as antibody-mediated abrogation of Dkk3 led to reduced tubular atrophy and decreased interstitial matrix accumulation in two mouse models of renal fibrosis. This was accompanied by an amplified, anti-fibrogenic, inflammatory response within the injured kidney. Mechanistically, Dkk3 deficiency led to diminished canonical Wnt/β-catenin signaling in stressed tubular epithelial cells. To identify global changes in gene expression due to the lack of Dkk3, whole-transcriptome sequencing (mRNA-seq) was performed on RNA isolated from kidneys of Wt and Dkk3-/- mice 7 days after UUO.

2016-01-20 | GSE75925 | GEO

Blood gene expression at 3 months post-transplantation predicts 1-year histologic features in renal transplantation

Project description:Histological analysis of biopsy is the gold standard to assess renal allograft status. Furthermore, 1-year protocol biopsy is often performed to evaluated graft outcome. However, since biopsy cannot be performed in a time serial basis, we decided to investigate whether blood can be a good compartment to predict allograft outcome. Gene expression microarrays and a large phenotype have been performed in peripheral blood mononuclear cells from 79 renal transplanted patients taken 3 months after transplantation. We evaluated the association of biological parameters with 4 histological groups defined on renal biopsy taken at 1-year post-transplantation: patients which display normal biopsy (n=45), patients with signs of tubular atrophy and interstitial fibrosis (IFTA) (n=14), with IFTA with inflammation (i-IFTA) (n=14) and patients with alloimmune lesions (n=6) Transcriptomic profile using PBMC from patients showing normal biopsy (n=45), patients with signs of tubular atrophy and interstitial fibrosis (IFTA) (n=14), with IFTA with inflammation (i-IFTA) (n=14) and patients with alloimmune lesions (n=6).

2015-12-24 | E-GEOD-57731 | biostudies-arrayexpress

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