Cyclosporine A timecourse 0, 12, 48 hours
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE1403 | GEO | 2004/12/20
SECONDARY ACCESSION(S): PRJNA90187
REPOSITORIES: GEO
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Project description:Effect of 4.2 micromolar Cyclosporine A on human renal proximal tubular cell line HK-2 over 48 hours
2008-06-11 | E-GEOD-1403 | biostudies-arrayexpress
Project description:K562 cells (duplicate cultures A & B) are treated with 50 micromolar hemin for 0, 6, 12, 24, 48, 72 hours followed by RNA extraction and gene expression profiling on Affymetrix human U133A arrays and analysis by MAS 5.0 Keywords: other
2004-04-05 | GSE1036 | GEO
Project description:To elucidate the gene profile of anti-fibroproliferative effects of cyclosporine, we added TGF-b and/or CsA to MRC5 (fetal human lung fibroblast) cell line. After 24 hours serum starvation, fibroblasts were treated with 3 ng/ml TGF-β1 and were treated with or without 2μg/ml Cyclosporine and effects were examined at 48 hours after treatment. Expression of three genes (IGFBP3, ID1 and PPARG) from this signature was quantified in the same RNA samples by real-time PCR. TGF-β and cyclosporine induced gene expression data was measured in MRC5 (fetal human fibroblast cell line) at 48h after treatments. The dose of TGF-β was 3 ng/ml and cyclosporine was 2 μg/ml. The comparison was done between four groups (control, TGF-β, cyclosporine and TGF-β plus cyclosporine).Three independent experiments were performed at each treatments using different samples for each experiment.
2010-11-09 | E-GEOD-25200 | biostudies-arrayexpress
Project description:Background- CINAC-patients can be identified by the recently discovered renal proximal tubular cell lysosomal lesions which are also observed in patients experiencing calcineurin inhibitor (CNI) nephrotoxicity, suggesting that CINAC is a toxin-induced nephropathy. An alternative hypothesis advocates chronic heat stress/dehydration as the major etiological factor for CINAC. Here, we evaluated in rats to what extent heat stress/dehydration reflects the renal CINAC histopathology in humans. Methods- Wistar rats were divided in 3 groups. Group 1(n=6) had free access to drinking water (control group). Group 2(n=8) was water deprived for 10 hours per 24hr, 5 days/week and placed in an incubator (37°C) for 30 min/hr during water deprivation. Group 3(n=8) underwent daily oral gavage with cyclosporine (40mg/kg body weight). After 28 days kidneys were collected for light- and electron microscopic histopathology and proteomic analysis. Results- Cyclosporine rats developed renal cortical lesions mimicking those of CINAC patients i.e. atrophic proximal tubules with associated tubulo-interstitial fibrosis. PASM staining demonstrated enlarged argyrophilic granules in the affected proximal tubules, identified as lysosomes by LAMP1 immunofluorescent staining. Electron microscopy confirmed the presence of enlarged dysmorphic lysosomes, closely mimicking the dysmorphic lysosomes seen in CINAC-patients. Dehydration was demonstrated by urinary osmolality and fluctuating body weight but showed none of the histological features of CINAC patients. Proteomic analysis confirmed cellular toxicity of cyclosporine, whereas the dehydration group lacked any of these toxicity markers. Conclusion- Dehydration/heat stress alone does not lead to the renal proximal tubular and interstitial lesions as observed in CINAC-patients. The histopathological analogy between CINAC and CNI nephrotoxicity in rats and humans and CINAC supports the toxicological etiology.
2022-11-14 | PXD038062 | Pride
Project description:To elucidate the gene profile of anti-fibroproliferative effects of cyclosporine, we added TGF-b and/or CsA to MRC5 (fetal human lung fibroblast) cell line. After 24 hours serum starvation, fibroblasts were treated with 3 ng/ml TGF-β1 and were treated with or without 2μg/ml Cyclosporine and effects were examined at 48 hours after treatment. Expression of three genes (IGFBP3, ID1 and PPARG) from this signature was quantified in the same RNA samples by real-time PCR.
2010-11-09 | GSE25200 | GEO
Project description:Investigate if one-pot analysis works on several energetic-based proteomics method on cyclosporine A.
2021-09-08 | PXD014309 | Pride
Project description:To investigate the effect of changes in oxygen tension and treatment with cyclosporine A on the chemotactic migration of B cells, we grew RAMOS B cells at 19% and 1% oxygen levels, and at 19% and 1% oxygen levels after treatment with cyclosporine A. We then performed RNA-seq on these RAMOS B cells and subequently gene expression profiling analysis on this RNA-seq data.
2023-02-13 | GSE212853 | GEO
Project description:Comparison of a cyclosporine-resistant murine CD8 T cell clone to a cyclosporine-sensitive murine T cell clone during activation (CSA = Cyclosporine A) Chronic allograft rejection is the leading cause of morbidity/mortality in solid organ and bone marrow transplant patients. It occurs in the setting of potent calcineurin and mTOR inhibitor therapies, implying that T cells mediating chronic rejection can function with compromised calcineurin-NFAT or IL-2 receptor signaling pathways. In murine models the T cells mediating allograft rejection in the setting of calcineurin inhibitor therapy are CD8 T cells making IFN-gamma without a requirement for perforin. It is not known whether these pathologic T cells are a unique subset or how they function. In parallel other animal model research has shown that alloepthelial cells residing in the donor organ are critical targets for rejection. While investigating T cell-alloepithelial cell interactions, we discovered an unusual alloreactive CD8 T cell population that recognized MHC class II I-Abm12. A CD8 T cell clone derived from that population was intrinsically-resistant to cyclosporine and rapamycin without prior exposure to either in vivo or in vitro. Microarray analysis comparing the novel CD8 T cell clone to a conventional CD8 CTL clone specific for MHC class I Kbm1 suggested that the TCR signaling pathway responsible for cyclosporine-resistance utilized the Aryl Hydrocarbon Receptor (AHR).
2014-04-14 | GSE46122 | GEO
Project description:Shotgun time-series proteomic analysis based on stable isotope dimethyl labeling and UHPLC-MS/MSC to relatively quantify the changes in protein expression of human proximal tubular HK-2 cells exposed to a diabetic-like microenvironment
2021-09-08 | PXD015102 | Pride
Project description:Comparison of a cyclosporine-resistant murine CD8 T cell clone to a cyclosporine-sensitive murine T cell clone during activation (CSA = Cyclosporine A) Chronic allograft rejection is the leading cause of morbidity/mortality in solid organ and bone marrow transplant patients. It occurs in the setting of potent calcineurin and mTOR inhibitor therapies, implying that T cells mediating chronic rejection can function with compromised calcineurin-NFAT or IL-2 receptor signaling pathways. In murine models the T cells mediating allograft rejection in the setting of calcineurin inhibitor therapy are CD8 T cells making IFN-gamma without a requirement for perforin. It is not known whether these pathologic T cells are a unique subset or how they function. In parallel other animal model research has shown that alloepthelial cells residing in the donor organ are critical targets for rejection. While investigating T cell-alloepithelial cell interactions, we discovered an unusual alloreactive CD8 T cell population that recognized MHC class II I-Abm12. A CD8 T cell clone derived from that population was intrinsically-resistant to cyclosporine and rapamycin without prior exposure to either in vivo or in vitro. Microarray analysis comparing the novel CD8 T cell clone to a conventional CD8 CTL clone specific for MHC class I Kbm1 suggested that the TCR signaling pathway responsible for cyclosporine-resistance utilized the Aryl Hydrocarbon Receptor (AHR). Two T cell clones x 2 experimental conditions x 4 replicates
2014-04-14 | E-GEOD-46122 | biostudies-arrayexpress