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MicroRNA expression profile of human umbilical vein endothelial cells in response to Coxsackievirus A10 infection

ABSTRACT: Coxsackievirus A10 (CV-A10) constitutes one of the major pathogens of hand, foot, and mouth disease (HFMD), which can cause mild to severe illness and even death. Most of these severe and death cases were closely associated with their neurological impairments, but the underlying mechanism of neuropathological injury induced by CV-A10 infection has not been elucidated. MicroRNAs (miRNAs), implicated in the regulation of gene expression in a posttranscriptional manner, play a vital role in the pathogenesis of various central nervous systems (CNS) diseases; thereby they are served as diagnostic biomarkers and are emerging as novel therapeutic targets for CNS injuries. To gain insights in the CV-A10-induced regulation of host miRNA-processing machinery, we employed high-throughput sequencing to identify differentially expressed miRNAs in CV-A10-infected HUVEC cells and further analyzed the potential functions of these miRNAs during CV-A10 infection. The results showed that CV-A10 infection could elicit 189 and 302 significantly differentially expressed miRNAs in HUVEC cells at 24 hpi and 72 hpi, respectively, as compared with the uninfected control.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236620 | GEO | 2023/07/26

REPOSITORIES: GEO

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Project description:ABSTRACT: Viral aseptic meningitis is a neuroinflammatory condition that occurs when viruses gain access to the central nervous system (CNS) and induce inflammation. The blood–brain barrier (BBB) is comprised of brain endothelial cells (BECs) that stringently regulate the passage of molecules, toxins, and pathogens from the circulation into the CNS. Through their unique properties, such as complex tight junctions, reduced rates of endocytosis, expression of efflux transporters, and restricted expression of leukocyte adhesion molecules, the BBB is often able to limit pathogen entry into the brain; however, certain neurotropic pathogens, such as coxsackievirus B3 (CVB3) are able to infect the CNS. We have previously demonstrated that CVB3 can infect and disrupt induced pluripotent stem cell-derived brain-like endothelial cells (iBECs), but the host response to this infection remains unknown. Here, we investigate global host transcriptional changes during CVB3 infection of iBECs using RNA sequencing. We validated our data set by exploring pathways altered by CVB3 using quantitative real-time PCR (qPCR) and enzyme-linked immunosorbent assay of upregulated cytokines and interferon signaling molecules. IMPORTANCE: Coxsackievirus B3 (CVB3) is a leading cause of viral aseptic meningitis that can cause severe disease in susceptible individuals. To gain access to the central nervous system, CVB3 must cross central nervous system barriers, such as the blood– brain barrier. Previously, we have shown that CVB3 infects a human stem cell-derived brain-like endothelial cell model. Here, we report the global transcriptome of stem cell-derived brain-like endothelial cells to CVB3 infection and provide proof-of-concept validation of the dataset using molecular biology techniques. These data could inform novel mechanisms of CVB3-mediated blood–brain barrier dysfunction. KEYWORDS: Coxsackievirus B3, blood-brain barrier, brain endothelial cells, RNA sequencing, induced pluripotent stem cells

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MicroRNA expression profile of human umbilical vein endothelial cells in response to Coxsackievirus A10 infection

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