Persistent Coxsackievirus B1 infection results in extensive changes in the transcriptome of a pancreatic cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766625 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16086128.fastq.gz | Fastqsanger.gz | |||
| SRR16086129.fastq.gz | Fastqsanger.gz | |||
| SRR16086130.fastq.gz | Fastqsanger.gz | |||
| SRR16086131.fastq.gz | Fastqsanger.gz | |||
| SRR16086132.fastq.gz | Fastqsanger.gz |
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Project description:The group B Coxsackieviruses can establish persistent infections in human cells, and these infections have been linked to chronic diseases including type 1 diabetes. Still, only little is known about persistent Coxsackievirus B infection induced changes in human pancreas. We have established persistent Coxsackievirus B1 infections in human pancreatic duct cell line using two different virus strains, and studied infection-induced changes in protein secretion using mass spectrometry-based proteomics. Persistent Coxsackievirus B1 infections caused broad changes in protein secretion, for example changes regulated secretory pathway. Strikingly, many changes differed between the virus strains, including extensive shut down of antiviral immune responses by one of the viruses. Our results provide novel information about persistent Coxsackievirus B infection induced changes in human pancreas and about the potential heterogeneity in the outcomes of the infections.
2019-08-06 | PXD012154 | Pride
Project description:Enteroviruses, particularly the group B Coxsackieviruses have been associated with the development of type 1 diabetes. Several CVB serotypes can establish chronic infection in human cells in vivo and in vitro. However, the mechanisms of leading to enterovirus persistency and, possibly, bell-cell autoimmunity are not fully understood. We established a carrier-state persistent infection model in human pancreatic ductal-like cell line PANC-1 using two distinct CVB1 strains and profiled infection-induced changes in cellular transcriptome. In the current study we observed clear changes in the gene expression of factors associated with the pancreatic microenvironment, the secretory pathway and lysosomal biogenesis during persistent CVB1 infections. Moreover, we gained deeper insights into immune-related genes which differed clearly between the two persistent infections. Overall our study reveals extensive transcriptional responses in persistently CVB1 infected pancreatic cell line with strong opposite but also common changes between the two strains.
2021-12-15 | GSE184831 | GEO
Project description:In human cells, the group B Coxsackieviruses can establish persistent infections that have been linked to chronic diseases including type 1 diabetes. Still, only little is known about the changes induced by persistent Coxsackievirus B infection in human pancreas. We have established persistent Coxsackievirus B1 infections in human pancreatic duct cell line using two different virus strains, and studied the consequences of these infections on intracellular protein expression using mass spectrometry-based proteomics. Persistent Coxsackievirus B1 infections caused broad changes in protein expression, for example changes in mitochondrial morphology and energy metabolism and in proteins associated with differentiation and survival of pancreatic beta-cells. Strikingly, many of these changes differed between the virus strains, including extensive shut down of antiviral immune responses by one of the viruses. Our results provide novel information about the changes induced by persistent Coxsackievirus B infection in human pancreas and about the potential heterogeneity in the outcomes of the infections.
2019-08-06 | PXD012153 | Pride
Project description:Enteroviruses, particularly the group B coxsackieviruses (CVBs), have been associated with the development of type 1 diabetes. Several CVB serotypes establish chronic infections in human cells in vivo and in vitro. However, the mechanisms leading to enterovirus persistency and, possibly, beta cell autoimmunity are not fully understood. We established a carrier-state-type persistent infection model in human pancreatic cell line PANC-1 using two distinct CVB1 strains and profiled the infection-induced changes in cellular transcriptome. In the current study, we observed clear changes in the gene expression of factors associated with the pancreatic microenvironment, the secretory pathway, and lysosomal biogenesis during persistent CVB1 infections. Moreover, we found that the antiviral response pathways were activated differently by the two CVB1 strains. Overall, our study reveals extensive transcriptional responses in persistently CVB1-infected pancreatic cells with strong opposite but also common changes between the two strains.
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Project description:Chronic exposure to aflatoxin B1 (AFB1) has, in certain regions in the world, been strongly associated with the development of hepatocellular carcinoma (HCC). AFB1 is a very potent hepatotoxic and carcinogenic mycotoxin which is frequently reported as a food contaminant. Epigenetic modifications provoked by environmental exposures, such as AFB1, may create a so called persistent "epigenetic memory" or "footprint". Deregulation of epigenetic mechanisms has actually been reported in HCC patients following AFB1 exposure; however no attempts have yet been made to investigate early effects on the epigenome level which may be persistent on longer term thereby possibly initiating carcinogenic events. In this study, we aim to identify methyl DNA-mRNA-interactions representative for a persistent epigenetic "footprint" associated with the early onset of AFB1-induced HCC. For this, primary human hepatocytes were exposed to 0.3 µM of AFB1 for 5 days. Persistent epigenetic effects were m easured 3 days after terminating the carcinogenic treatment. Whole genome DNA methylation changes and whole genome transcriptomic analysis were analyzed applying microarray technologies, and cross-omics interactions were evaluated. Upon combining transcriptomics data with results on DNA methylation, a range of persistent hyper- and hypomethylated genes was identified which appeared also affected on the transcriptome level. For six of the hypomethylated and upregulated genes, namely TXNRD1, PCNA, CCNK, DIAPH3, RAB27A and HIST1H2BF, a clear role in carcinogenic events could be identified. This study is the first to report on a carcinogen-induced persistent impact on the "epigenetic footprint" in relation with the transcriptome which could be indicative for the early onset of AFB1-related development of HCC.
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Project description:Chronic exposure to aflatoxin B1 (AFB1) has, in certain regions in the world, been strongly associated with the development of hepatocellular carcinoma (HCC). AFB1 is a very potent hepatotoxic and carcinogenic mycotoxin which is frequently reported as a food contaminant. Epigenetic modifications provoked by environmental exposures, such as AFB1, may create a so called persistent "epigenetic memory" or "footprint". Deregulation of epigenetic mechanisms has actually been reported in HCC patients following AFB1 exposure; however no attempts have yet been made to investigate early effects on the epigenome level which may be persistent on longer term thereby possibly initiating carcinogenic events. In this study, we aim to identify methyl DNA-mRNA-interactions representative for a persistent epigenetic "footprint" associated with the early onset of AFB1-induced HCC. For this, primary human hepatocytes were exposed to 0.3 µM of AFB1 for 5 days. Persistent epigenetic effects were m easured 3 days after terminating the carcinogenic treatment. Whole genome DNA methylation changes and whole genome transcriptomic analysis were analyzed applying microarray technologies, and cross-omics interactions were evaluated. Upon combining transcriptomics data with results on DNA methylation, a range of persistent hyper- and hypomethylated genes was identified which appeared also affected on the transcriptome level. For six of the hypomethylated and upregulated genes, namely TXNRD1, PCNA, CCNK, DIAPH3, RAB27A and HIST1H2BF, a clear role in carcinogenic events could be identified. This study is the first to report on a carcinogen-induced persistent impact on the "epigenetic footprint" in relation with the transcriptome which could be indicative for the early onset of AFB1-related development of HCC.
2016-05-10 | GSE71545 | GEO
Project description:Chronic exposure to aflatoxin B1 (AFB1) has, in certain regions in the world, been strongly associated with the development of hepatocellular carcinoma (HCC). AFB1 is a very potent hepatotoxic and carcinogenic mycotoxin which is frequently reported as a food contaminant. Epigenetic modifications provoked by environmental exposures, such as AFB1, may create a so called persistent "epigenetic memory" or "footprint". Deregulation of epigenetic mechanisms has actually been reported in HCC patients following AFB1 exposure; however no attempts have yet been made to investigate early effects on the epigenome level which may be persistent on longer term thereby possibly initiating carcinogenic events. In this study, we aim to identify methyl DNA-mRNA-interactions representative for a persistent epigenetic "footprint" associated with the early onset of AFB1-induced HCC. For this, primary human hepatocytes were exposed to 0.3 µM of AFB1 for 5 days. Persistent epigenetic effects were m easured 3 days after terminating the carcinogenic treatment. Whole genome DNA methylation changes and whole genome transcriptomic analysis were analyzed applying microarray technologies, and cross-omics interactions were evaluated. Upon combining transcriptomics data with results on DNA methylation, a range of persistent hyper- and hypomethylated genes was identified which appeared also affected on the transcriptome level. For six of the hypomethylated and upregulated genes, namely TXNRD1, PCNA, CCNK, DIAPH3, RAB27A and HIST1H2BF, a clear role in carcinogenic events could be identified. This study is the first to report on a carcinogen-induced persistent impact on the "epigenetic footprint" in relation with the transcriptome which could be indicative for the early onset of AFB1-related development of HCC.
2016-05-10 | GSE71548 | GEO