Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA877646 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21465858.fastq.gz | Fastqsanger.gz | |||
| SRR21465859.fastq.gz | Fastqsanger.gz | |||
| SRR21465860.fastq.gz | Fastqsanger.gz | |||
| SRR21465861.fastq.gz | Fastqsanger.gz | |||
| SRR21465862.fastq.gz | Fastqsanger.gz |
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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:Background: Hypoxia is a potent molecular signal for cellular metabolism, mitochondrial function, and migration. Conditions of low oxygen tension trigger regulatory cascades mediated via the highly conserved HIF-1 α post-translational modification system. In the adaptive immune response, B cells (Bc) are activated and differentiate under hypoxic conditions within lymph node germinal centers, and subsequently migrate to other compartments. During migration, they traverse through changing oxygen levels, ranging from 1-5% in the lymph node to 5-13% in the peripheral blood. Interestingly, the calcineurin inhibitor cyclosporine A is known to stimulate prolyl hydroxylase activity, resulting in HIF-1 α destabilization and may alter Bc responses directly. Over 60% of patients taking calcineurin immunosuppressant medications have hypo-gammaglobulinemia and poor vaccine responses, putting them at high risk of infection with significantly increased morbidity and mortality. Results: We demonstrate that oxygen tension is a previously unrecognized Bc regulatory switch, altering CXCR4 and CXCR5 chemokine receptor signaling in activated Bc through HIF-1 α expression, and controlling critical aspects of Bc migration. Our data demonstrate that calcineurin inhibition hinders this oxygen regulatory switch in primary human Bc. Conclusion: This previously unrecognized effect of calcineurin inhibition directly on human Bc has significant and direct clinical implications.
2023-07-20 | PXD037004 | 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. 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: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:Effect of PT2385 treatment during cytotrophoblast differentiation under hypoxia
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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:Infection of Gram-negative bacteria in female genital tract causes systematic immune-response and reproductive dysfunction. Immunosuppressor Cyclosporine A (CsA) is widely used in the treatment of genital tract immune response, however, the knowledge on the changes of transcriptome after CsA inhibiting lipopolysaccharide (LPS)-induced immune response still remains unknown.
2020-06-13 | GSE152343 | GEO
Project description:Effect of 4.2 micromolar Cyclosporine A on human renal proximal tubular cell line HK-2 over 48 hours Keywords: time-course
2004-12-20 | GSE1403 | GEO
Project description:After 2 and 12 weeks of treatment, we observed significant reductions of 51% and 72%, respectively, in SCORAD scores. Clinical improvements were associated with significant gene expression changes in lesional but also nonlesional skin, particularly reductions in levels of TH2-, TH22-, and some TH17-related molecules (ie, IL-13, IL-22, CCL17, S100As, and elafin/peptidase inhibitor 3), and modulation of epidermal hyperplasia and differentiation measures. Cyclosporine A (CsA)'s effects on AD skin pathology were evaluated by using gene expression and immunohistochemistry studies in baseline, week 2, and week 12 lesional and nonlesional biopsy specimens from 19 patients treated with 5 mg/kg/day CsA for 12 weeks.
2014-06-17 | E-GEOD-58558 | biostudies-arrayexpress
Project description:Chemotaxis is used by free-living motile bacteria to swim towards nutrient sources or away from repellents, and to navigate the environment to locate niches optimal for growth and survival. Multiple chemotaxis systems have been identified in different bacterial species, including Azospirillum brasilense. In A. brasilense, chemotaxis is mediated by two distinct chemotaxis pathways, named Che1 and Che4, that physically interact to form mixed chemotaxis signaling arrays. Signaling from the Che1 and Che4 pathways control transient increases in swimming speed and swimming reversals, respectively, during chemotaxis. In A. brasilense, chemotaxis is tightly linked to energy metabolism with this coupling occurring through the sensory input of several energy-sensing chemoreceptors and through the control of chemoreceptor activity by the c-di-GMP second messenger. Previous work has demonstrated that chemotaxis in A. brasilense also affects unrelated cellular functions including cell-to-cell clumping and flocculation. However, the molecular mechanism for these effects is not known. Here, we identify additional effects of mutations abolishing Che1 (cheA1 mutant), Che4 (cheA4 mutant) or both Che1 and Che4 (cheA1/cheA4 mutant) function on nitrogen and carbon metabolism and use whole cell proteome and metabolome mass spectrometry to further characterize the interplay between chemotaxis and metabolism. We found that CheA1 mediates most changes in chemoreceptor arrays composition and also affects small molecules signaling while a mutant lacking CheA4 displays changes in nitrogen metabolism, including nitrate assimilation and nitrogen fixation. In contrast, the mutant lacking both CheA1 and CheA4, which lacks chemotaxis and does not form chemotaxis signaling arrays, displays distinct and non-overlapping changes that suggest the assembly of chemotaxis signaling arrays modulates energy and carbon metabolism. Together, the results suggest distinct roles for CheA1, CheA4 and chemotaxis signaling arrays in modulating chemotaxis and metabolism, likely through control of distinct global regulatory networks.
2020-08-25 | MSV000086008 | MassIVE