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Gene expression data from endothelial cells and leukocytes enriched from transplanted rat hearts

ABSTRACT: Transcriptome analyses of organ transplants have until now usually focused on whole tissue samples containing activation profiles from different cell populations. Here, we enriched endothelial cells from rat cardiac allografts and isografts, establishing their activation profile at baseline and on day 2, 3 and 4 after transplantation. Modulated transcripts were assigned to three categories based on their regulation profile in allografts and isografts. Categories A and B contained the majority of transcripts and showed similar regulation in both graft types, appearing to represent responses to surgical trauma. By contrast, category C contained transcripts that were partly allograft-specific and to a large extent associated with interferon-gamma-responsiveness. Several transcripts were verified by immunohistochemical analysis of graft lesions, among them the matricellular protein periostin which was one of the most highly upregulated transcripts but has not been associated with transplantation previously. In conclusion, the majority of the differentially expressed genes in graft endothelial cells are affected by the transplantation procedure whereas relatively few are associated with allograft rejection.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE16695 | GEO | 2010/07/06

SECONDARY ACCESSION(S): PRJNA117379

REPOSITORIES: GEO

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Gene expression data from endothelial cells and leukocytes enriched from transplanted rat hearts

Project description:Transcriptome analyses of organ transplants have until now usually focused on whole tissue samples containing activation profiles from different cell populations. Here, we enriched endothelial cells from rat cardiac allografts and isografts, establishing their activation profile at baseline and on day 2, 3 and 4 after transplantation. Modulated transcripts were assigned to three categories based on their regulation profile in allografts and isografts. Categories A and B contained the majority of transcripts and showed similar regulation in both graft types, appearing to represent responses to surgical trauma. By contrast, category C contained transcripts that were partly allograft-specific and to a large extent associated with interferon-ï§-responsiveness. Several transcripts were verified by immunohistochemical analysis of graft lesions, among them the matricellular protein periostin which was one of the most highly upregulated transcripts but has not been associated with transplantation previously. In conclusion, the majority of the differentially expressed genes in graft endothelial cells are affected by the transplantation procedure whereas relatively few are associated with allograft rejection. Endothelial cells were enriched from control/non-transplanted hearts and from allografts (DA to Lewis) and isografts (Lewis to Lewis) harvested at day 2, 3 and 4 after transplantation. Three biological replicates from each time point and graft type were analyzed (a total of 24 arrays). Leukocytes were enriched from allografts at day 2 (n=1), day 3 (n=2) and day 4 (n=1) after transplantation.

2010-07-29 | E-GEOD-16695 | biostudies-arrayexpress

Identification of microRNAs involved in acute rejection and spontaneous tolerance in murine hepatic allografts

Project description:Graft acceptance without the need for immunosuppressive drugs is the ultimate goal of transplantation therapy. In murine liver transplantation, allografts are accepted across major histocompatibility antigen complex barriers without the use of immunosuppressive drugs and constitute a suitable model for research on immunological rejection and tolerance. MicroRNA (miRNA) has been known to be involved in the immunological responses. In order to identify mRNAs in spontaneous liver allograft tolerance, miRNA expression in hepatic allografts was examined using this transplantation model. According to the graft pathological score and function, miR-146a, 15b, 223, 23a, 27a, 34a and 451 were upregulated compared with the expression observed in the syngeneic grafts. In contrast, miR-101a, 101b and 148a were downregulated. Our results demonstrated the alteration of miRNAs in the allografts and may indicate the role of miRNAs in the induction of tolerance after transplantation. Furthermore, our data suggest that monitoring the graft expression of novel miRNAs may allow clinicians to differentiate between rejection and tolerance. A better understanding of the tolerance inducing mechanism observed in murine hepatic allografts may provide a therapeutic strategy for attenuating allograft rejection.

2014-10-21 | GSE52164 | GEO

Identification of microRNAs involved in acute rejection and spontaneous tolerance in murine hepatic allografts

2014-10-21 | E-GEOD-52164 | biostudies-arrayexpress

Leukocyte accumulation in graft blood vessels during self-limiting acute rejection of rat kidneys Immunobiology

Project description:Acute rejection episodes trigger chronic renal allograft vasculopathy. Numerous leukocytes, predominantly monocytes, accumulate in graft blood vessels during reversible acute rejection preceding chronic rejection of rat kidneys. We speculate that they contribute to transplant vasculopathy and set out to characterize them. Allogeneic renal transplantation was performed in the Fischer 344 to Lewis rat strain combination, Lewis isografts served as controls. Leukocytes were harvested by intensive perfusion of graft blood vessels and subjected to flow cytometry, quantitative RT-PCR and genome-wide transcriptional profiling. Kidneys of LEW and F344 rats were transplanted in LEW rats. Five biological replicates were performed for both isogenic and allogenic transplantation. Transcriptomes of allogenics were compared to isogenics on 5 dual-color hybridizations.

2010-09-24 | E-GEOD-18266 | biostudies-arrayexpress

Resident memory T cells form during persistent antigen exposure leading to allograft rejection

Project description:Tissue resident memory T cells (TRM) contained at sites of previous infection provide local protection against re-infection. Whether they form and function in organ transplants where cognate antigen persists is unclear. This is a key question in transplantation as T cells are detected long-term in allografts, but it is not known whether they are exhausted or are functional memory T cells. Using a mouse model of kidney transplantation, we showed that antigen-specific and polyclonal effector T cells differentiated in the graft into TRM and subqeuntly caused allograft rejection. TRM identity was established by surface phenotype, transcriptional profile, and inability to recirculate in parabiosis and re-transplantation experiments. Graft TRM proliferated locally, produced IFNγ upon re-stimulation, and their in vivo depletion attenuated rejection. Importantly, the vast majority of antigen-specific and polyclonal TRM lacked phenotypic and transcriptional exhaustion markers. Single cell analysis of graft T cells early and late after transplantation identified a transcriptional program associated with transition to the tissue resident state that could serve as a platform for the discovery of therapeutic targets. Thus, recipient effector T cells differentiate into functional graft TRM that maintain rejection locally. Targeting these TRM could improve renal transplant outcomes.

2021-03-20 | GSE166166 | GEO

Leukocyte accumulation in graft blood vessels during self-limiting acute rejection of rat kidneys Immunobiology

2010-09-24 | GSE18266 | 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

Transcription profiling of tolerizing murine cardiac allograft to understand the precise mechanisms of immunological tolerance.

Project description:C57/BL6 to C57/BL6; Balb/c to C57/BL6; Balb/c to C57/BL6 with anti CD80/86 mAb; Identificaton of gene expression profile in tolerizing murine cardiac allograft by co-stimulatory blockade. The induction of specific tolerance would be the ultimate achievement in transplant immunology, but the precise mechanisms of immunological tolerance remain largely unknown. Here, we investigated global gene expression analysis in tolerizing murine cardiac allografts by means of oligonucleotide microarrays. Tolerance induction was achieved in cardiac allografts from BALB/c to C57BL/6 mice by daily intraperitoneal injection of anti-CD80 and CD86 mAbs. Comparative analysis revealed 64 genes to be induced more extensively in the tolerizing than in the syngeneic isografts, and 16 genes than in the rejecting allografts. Two genes were specifically upregulated in the tolerizing allografts. In the tolerizing allografts there were induced marked expressions of a number of genes for proinflammatory factors, including interferon-gamma inducible cytokines and chemokines, as well as apoptosis-related genes which were also upregulated in the rejecting allografts. Moreover, these gene expression patterns continued to be upregulated more than 70 days post transplant. These results provide evidence that immunological tolerance can be induced and maintained in the presence of prominent proinflammatory gene expression in vivo.

2007-12-15 | E-GEOD-582 | biostudies-arrayexpress

The Atlas of Immune Infiltrates in Islet Cell Allo-transplantation

Project description:Islet transplantation to treat the late stage of T1DM patients has made some inspiring success recently in clinical trials. However, most of patients underwent a decline of islet cell graft in one to three years due to chronic immune rejection. Although the mechanisms of immune cells including macrophages, dendritic cells (DCs), neutrophils, natural killer cells (NKs), B cells, T cells that mediate immune rejection have been investigated, the overall characteristics of immune infiltrates in islet allografts remain unclear. Single-cell RNA sequencing (scRNA-seq) has provided us with new opportunities to study the molecular characteristics of the immune microenvironment in islet transplants. In the present study, we used scRNA-seq to comprehensively analyze the immune heterogeneity in islet graft, and compared the variances regarding to transcriptomal profiling and immune atlas between syngeneic islet transplantation and allograft.

2022-05-25 | GSE198865 | GEO

Analysis of graft-infiltrating CD8+ T cell profile after CD3 antibody therapy

Project description:We performed a global gene expression analysis comparing intragraft tolerant CD8+ T cells from CD3 antibody-treated mice showing permanent islet graft survival to intra-graft effector CD8+ T cells isolated from untreated mice showing acute rejection of islet allografts. The objective was to emphasize the anergic profile of CD8+ T cells residing within the pancreatic islet allograft of mice rendered tolerant following CD3 antibody therapy.

2017-02-10 | GSE68208 | GEO

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