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Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells

ABSTRACT: Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells

PROVIDER: PRJNA877646 | ENA |

REPOSITORIES: ENA

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			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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Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells

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

Effect of hypoxia and treatment with cyclosporine A on chemotaxis of RAMOS B cells

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

Effect of expression of ZEBRA on gene expression during Ramos cells

Project description:EBV immediate early protein ZEBRA was corroborated to interact with Pax5 which controls the fate of B cells. Ramos cells were infected with ZEBRA-expression lentivirus and positively infected cells were sorted, which were named Ramos-Lv-ZEBRA.

2024-04-24 | GSE264391 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Ramos and Rituximab-resistant Ramos cell Transcriptomes

Project description:The goal of this study is to screen the differential genes between Ramos and Rituximab-resistant Ramos cells, then analyze the significant pathways.

2019-02-13 | GSE112592 | GEO

Effect of expression of ZEBRA on gene expression in Ramos cells [CUT-Tag]

2024-04-26 | GSE264476 | GEO

Effect of expression of ZEBRA on gene expression in Ramos cells [ChIP-Seq]

2024-04-26 | GSE264475 | GEO

Cyclosporine on fibroblast

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.

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Cyclosporine on fibroblast

2010-11-09 | GSE25200 | GEO

Rat Kidney MS analysis with dehydration and cyclosporine treatment

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

SP140 ChIP-seq for Daudi and Ramos cell lines

Project description:Study of the effect of SP140 deletion on the distribution of H3K27me3 in two independent Burkitt''s Lymphoma cell lines (DAUDI and Ramos).

2024-11-21 | GSE229801 | GEO

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