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Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation

ABSTRACT: Interactions between human cytomegalovirus (HCMV) infection and environmental factors can increase susceptibility to essential hypertension (EH). Although endothelial dysfunction is the initial factor of EH, the epigenetic mechanisms through which HCMV infection induces endothelial cell dysfunction are poorly understood. Here, we evaluated whether HCMV regulated endothelial cell function and assessed the underlying mechanisms. Microarray analysis in human umbilical vein endothelial cells (HUVECs) treated with HCMV AD169 strain in the presence of hyperglycemia and hyperlipidemia revealed differential expression of genes involved in hypertension.

ORGANISM(S): Homo sapiens

PROVIDER: GSE142762 | GEO | 2020/02/14

REPOSITORIES: GEO

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Human induced pluripotent stem cell-technology to study the effects of human cytomegalovirus infection on neural differentiation

Project description:Congenital human cytomegalovirus (HCMV) infection is one of the leading prenatal causes of mental retardation and congenital deformities world-wide. Access to cultured human neuronal lineages, necessary to understand the species specific pathogenic effects of HCMV has been limited by difficulties in sustaining primary cultures. Neuronal cells derived from human induced pluripotent stem (iPS) cells now provide a novel opportunity to investigate HCMV pathogenesis. We derived iPS cells from human adult fibroblasts and induced neural lineages to investigate their permissiveness to infection with HCMV strain Ad169. Analysis of iPS cells and nearly pure populations of iPS-derived neural stem cells (NSCs), neuroprogenitor cells (NPCs) and neurons suggests that (i) iPS cells are not permissive to HCMV infection; (ii) Neural stem cells have impaired differentiation when infected by HCMV; (iii) NPCs are fully permissive for HCMV infection; the supernatant from infected neural stem cells and NPCs (but not mock infected cells) induced cytopathic effects in human fibroblasts; (iv) most iPS-derived neurons are not permissive to HCMV infection; and (v) infected neurons have impaired calcium influx in response to glutamate. Our approach offers powerful cellular models to investigate the effect of neurotropic viral agents on human neurodevelopment. Adherent monolayer culture of neural progenitor cells (NPCs) were either infected with HCMV Ad169 in triplicate, with each individual sample harvested separately to provide biological replicates for expression analysis. Infected and mock-infected cells were harvested 24 h p.i. RNA. NPCs were 70-80% confluence.

2013-01-04 | E-GEOD-35295 | biostudies-arrayexpress

RNA-seq Transcriptome Analysis of AD169 and AD169-ΔUL26 infected MRC5 fibroblasts.

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Human induced pluripotent stem cell-technology to study the effects of human cytomegalovirus infection on neural differentiation

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RNA-seq transcriptome analysis of HCMV (AD169) and mock infected MRC5 fibroblasts

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Human cytomegalovirus protein pUL36: a dual cell death pathway inhibitor

Project description:Human cytomegalovirus (HCMV) is an important human pathogen and a paradigm of intrinsic, innate and adaptive viral immune evasion. Here, we employ multiplexed tandem mass tag-based proteomics to characterise host proteins targeted for degradation late during HCMV infection. This approach revealed that mixed lineage kinase domain-like protein (MLKL), a key terminal mediator of cellular necroptosis, was rapidly and persistently degraded by the minimally passaged HCMV strain Merlin but not the extensively passaged strain AD169. The strain Merlin viral inhibitor of apoptosis pUL36 was necessary and sufficient both to degrade MLKL and to inhibit necroptosis. Furthermore, mutation of pUL36 Cys131 abrogated MLKL degradation and restored necroptosis. As the same residue is also required for pUL36-mediated inhibition of apoptosis by preventing proteolytic activation of pro-caspase 8, we define pUL36 as a multifunctional inhibitor of both apoptotic and necroptotic cell death.

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Deletion of HCMV US17 alters host immune genes at 12 hpi and ER stress genes at 96 hpi.

Project description:Infection of human fibroblasts with either human cytomegalovirus strain AD169 or a recombinant virus deleted for HCMV US17 Illumina HT-12 beadarrays were used to quantitate levels of host transcripts at either 12 or 96 hpi.

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Deletion of HCMV US17 alters host immune genes at 12 hpi and ER stress genes at 96 hpi.

2013-11-30 | E-GEOD-50955 | biostudies-arrayexpress

Iron chelation on human cytomegalovirus infected MRC-5 fibroblasts

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2003-09-20 | GSE672 | GEO

Transcriptome profiling of human cytomegalovirus-infected trophoblasts

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2023-12-14 | GSE248772 | GEO

Human cytomegalovirus infection perturbs neural progenitor cell fate via the expression of viral microRNAs

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2023-06-30 | GSE206370 | GEO

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