Ontology highlight
ABSTRACT:
PROVIDER: PRJNA670723 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12880221.fastq.gz | Fastqsanger.gz | |||
| SRR12880222.fastq.gz | Fastqsanger.gz | |||
| SRR15354983.fastq.gz | Fastqsanger.gz | |||
| SRR15354984.fastq.gz | Fastqsanger.gz | |||
| SRR19614363.fastq.gz | Fastqsanger.gz |
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Project description:We study the global gene expression profiles of BKV viremia and nephropathy patients using microarrays in order to better understand the immunologic response to polyomavirus BK (BKV). BKV has become increasingly prevalent since the introduction of more potent immunosuppressive agents. It has been shown that as many as 30% of renal transplant recipients develop asymptomatic viral shedding in the urine shortly after transplant, 10-20% have viremia, and as many as 1-10% can go on to develop overt nephropathy (BKVN) that might lead to graft loss. To date, the genomics of BKV viremia and BKVN have not been investigated thoroughly by microarray. Patients who were enrolled in the IRB-approved Immune Monitoring Study had blood PAXGene samples taken at post-transplant visits and had clinically indicated biopsy samples were used for analysis. A total of 17 biopsy samples were used for gene expression profiling microarrays, three with histopathologic diagnosis of BKVN, 3 patients with evidence of BK viral replication in peripheral blood, but normal biopsy and 11 patients with normal biopsies or mild IFTA, and stable graft function. Blood PAXGene samples from 40 patients were used for gene expression profiling by microarrays, 14 patients with stable graft function and without BK viremia, 19 patients' blood samples at the time of BKV viremia, and 7 patients blood samples taken 1-2 months prior to development of BK viremia.
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Project description:Background Immunosuppressants and renal ischemia-reperfusion injury (IRI) are risk factors for BK polyomavirus infection after kidney transplantation. However, the mechanism remains unclear. Methods We used a model of mouse polyomavirus (MPyV) infection to investigate the mechanism of IRI and immunosuppressants to promote polyomavirus replication. Results After primary infection, MPyV established persistent infection in the kidneys until week 9 and subsequently were significantly increased by IRI or immunosuppressants treatment individually. In IRI group, viral loads peaked on day 3 in the left kidney, which were significantly higher than that in the right kidney and the control group, and then gradually decreased. In immunosuppressants group, viral loads increased on day 3 without significant difference between left and right kidney, which were significantly higher than that in the control group, and then maintained at high levels. Protein-protein interaction network analysis screened complement C3, EGFR, and FN1 as core genes. Pathway enrichment analysis based on the IRI or immunosuppressants related genes selected by WGCNA indicated that NF-?B signaling pathway was the main pathway involved in promoting MPyV replication. We further confirmed our findings using published datasets GSE47199 and GSE75693. Conclusions Our study demonstrated that IRI and immunosuppressants promote polyomavirus replication through common molecular mechanisms.
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Project description:Mutations in cancer are due in part to DNA cytosine deamination by APOBEC3B (A3B). While low in healthy tissues, A3B expression and activity are elevated in tumors and further increase in metastases. However, molecular mechanisms responsible for A3B transcriptional regulation are poorly understood. Here, we address whether the RB/E2F pathway, which is often dysregulated in breast cancer, is a molecular trigger of A3B overexpression. First, an A3B promoter-driven luciferase reporter was used to demonstrate reporter activation by disruption of only one out of five predicted E2F binding sites. Second, A3B-luciferase reporter activation was also triggered by expressing the BK polyomavirus T-antigen, which inactivates RB and thereby alleviates repression of E2F regulated genes. Importantly, A3B-luciferase reporter induction by BK polyomavirus T-antigen could not be further increased by mutating the functional E2F binding site. Third, both CRISPR disruption and targeted base substitutions in the endogenous E2F binding site caused strong A3B upregulation and confirmed importance of this regulatory element. Fourth, proteomics experiments showed that members of the DREAM and PRC1.6-complexes including multiple E2F family members are able to bind to wild-type but not E2F mutant promoter sequences. Finally, a combination of genetic and biochemical studies implicated E2F4 and E2F6 in endogenous A3B gene repression. Altogether, our studies demonstrate that A3B expression is suppressed in normal cells by the RB/E2F axis and that viral or mutational disruption of this pathway causes overexpression of this DNA deaminase in cancer and contributes mutational fuel to tumor evolution.
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