ArticleFEBS open bio2018
MicroR-9-5p suppresses EV71 replication through targeting NFκB of the RIG-I-mediated innate immune response.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- Retraction Note to: EV71 virus reduces Nrf2 activation to promote production of reactive oxygen species in infected cells.Gut pathogens · 2023Article
- MicroRNAs in the Regulation of RIG-I-like Receptor Signaling Pathway: Possible Strategy for Viral Infection and Cancer.Biomolecules · 2023Review
- Enterovirus 71 induces pyroptosis of human neuroblastoma SH-SY5Y cells through miR-146a/ CXCR4 axis.Heliyon · 2023Article
- The upregulation of peripheral blood polyamine metabolites spermidine and spermine in children with hand, foot, mouth disease is related to enterovirus 71 capsid protein VP1, but not VP4.Translational pediatrics · 2023Article
- Roles of Non-Coding RNAs in Virus-Host Interaction About Pathogenesis of Hand-Foot-Mouth Disease.Current microbiology · 2022Review
- Comparative transcriptomics reveals small RNA composition and differential microRNA responses underlying interferon-mediated antiviral regulation in porcine alveolar macrophages.Frontiers in immunology · 2022Article
- Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022Review
- Essential Role of Non-Coding RNAs in Enterovirus Infection: From Basic Mechanisms to Clinical Prospects.International journal of molecular sciences · 2021Review
- microRNA-9-5p protects liver sinusoidal endothelial cell against oxygen glucose deprivation/reperfusion injury.Open life sciences · 2021Article
- Downregulation of miR-155-5p facilitates enterovirus 71 replication through suppression of type I IFN response by targeting FOXO3/IRF7 pathway.Cell cycle (Georgetown, Tex.) · 2020Article
- Antivirals and vaccines for Enterovirus A71.Journal of biomedical science · 2019Review
- MicroRNA-221 inhibits human papillomavirus 16 E1-E2 mediated DNA replication through activating SOCS1/Type I IFN signaling pathway.International journal of clinical and experimental pathology · 2019Article
Corrections and comments
- Retraction · 2023-03-17Duplication of/in Article · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/D0786BCAA136B23C1500813F2B25AA
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence demonstrates that there is a causative link between hsa-microRNA-9-5p (miR-9) and pathophysiological processes. Enterovirus 71 (EV71) has been found to contribute to numerous severe clinical symptoms which result in death. The exact mechanism by which EV71 influences miR-9 expression is unknown, and the relationship between miR-9 and EV71 is still unclear. Here, miR-9 expression was found to be impaired upon EV71 infection in several cell lines and in an EV71 infection mouse model. Additionally, we confirmed that EV71 infection induces robust expression of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1) and interferons (IFN-α and IFN-β). Overexpression of miR-9 attenuated EV71 proliferation and reduced protein and gene expressions of virion protein 1 (VP1) of EV71. Furthermore, we observed that the inflammation caused by EV71 infection was restored to a moderate level via miR-9 overexpression. Nuclear factor kappa B (NFκB) in the retinoic acid-induced gene 1 (RIG-I) signaling pathway, but not interferon regulating factor 3 (IRF3), was significantly decreased and inactivated by ectopic miR-9 expression. Moreover, in mouse infection experiments, administration of miR-9 agomirs caused a significant decrease in VP1 levels and pro-inflammatory cytokine production after viral inoculation. Taken together, the present data demonstrate that miR-9 exerts an anti-EV71 effect in cells and a mouse model via mediating NFκB activity of the RIG-I signal pathway, thereby suggesting a new candidate for antiviral drug development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.