About: 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.   Goto Sponge  NotDistinct  Permalink

An Entity of Type : fabio:Abstract, within Data Space : covidontheweb.inria.fr associated with source document(s)

AttributesValues
type
value
  • 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.
subject
  • Virology
  • Immunostimulants
  • Enteroviruses
  • MicroRNA
  • Infraspecific virus taxa
  • MicroRNA precursor families
part of
is abstract of
is hasSource of
Faceted Search & Find service v1.13.91 as of Mar 24 2020


Alternative Linked Data Documents: Sponger | ODE     Content Formats:       RDF       ODATA       Microdata      About   
This material is Open Knowledge   W3C Semantic Web Technology [RDF Data]
OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2025 OpenLink Software