About: MicroR‐9‐5p suppresses EV71 replication through targeting NFκB of the RIG‐I‐mediated innate immune response

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About: MicroR‐9‐5p suppresses EV71 replication through targeting NFκB of the RIG‐I‐mediated innate immune response Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	MicroR‐9‐5p suppresses EV71 replication through targeting NFκB of the RIG‐I‐mediated innate immune response
Creator	Li, Bing Zheng, Junqing
topic	covid:620c2d071dd49eb5bcc31f378eb219310e4b1ebc#this
Source	Medline; PMC
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.
has issue date	2018-08-29(xsd:dateTime)
bibo:doi	10.1002/2211-5463.12490
bibo:pmid	30186747
has license	cc-by
sha1sum (hex)	620c2d071dd49eb5bcc31f378eb219310e4b1ebc
schema:url	https://doi.org/10.1002/2211-5463.12490
resource representing a document's title	MicroR‐9‐5p suppresses EV71 replication through targeting NFκB of the RIG‐I‐mediated innate immune response
has PubMed Central identifier	PMC6120239
has PubMed identifier	30186747
schema:publication	FEBS Open Bio
resource representing a document's body	covid:620c2d071dd49eb5bcc31f378eb219310e4b1ebc#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/620c2d071dd49eb5bcc31f378eb219310e4b1ebc
is schema:about of	named entity 'interferon' named entity 'virion' named entity 'mouse' named entity 'cell lines' named entity 'signal' named entity 'severe' named entity 'proliferation' named entity 'innate immune response' covid:arg/620c2d071dd49eb5bcc31f378eb219310e4b1ebc named entity 'cytokine' named entity 'result' named entity 'IL-1' named entity 'infection' named entity 'model' named entity 'expression' named entity 'signaling pathway' named entity 'mechanism' named entity 'pathway' named entity 'mouse' named entity 'VP1' named entity 'interferon' named entity 'RIG-I' named entity 'EV71' named entity 'miR-9' named entity 'clinical symptoms' named entity 'pro-inflammatory cytokine' named entity 'antiviral drug' named entity 'hsa' named entity 'IL-6' named entity 'miR-9' named entity 'signaling pathway' named entity 'IFN' named entity 'inflammation' named entity 'miR-9' named entity 'EV71' named entity 'miR-9' named entity 'miR-9' named entity 'EV71' named entity 'Nuclear' named entity 'Here' named entity 'development' named entity 'interleukin' named entity 'mouse model' named entity 'Ectopic expression' named entity 'protein' named entity 'viruses' named entity 'Tokyo' named entity 'cell lines' named entity 'miR-9' named entity 'miR-9' named entity 'RNA' named entity 'pro-inflammatory cytokine' named entity 'gene' named entity 'Virion' named entity 'Dulbecco's modified Eagle's medium' named entity 'transfection' named entity 'EV71' named entity 'expression patterns' named entity 'mice' named entity 'rhabdomyosarcoma' named entity 'EV71' named entity 'RLR' named entity 'innate immune response' named entity 'IL-1' named entity 'EV71' named entity 'viral RNA' named entity 'mRNA' named entity 'miR-9' named entity 'freeze-thaw' named entity 'miR-9' named entity 'EV71' named entity 'staining' named entity 'mice' named entity 'China' named entity 'b-galactosidase' named entity 'interferon' named entity 'mRNA' named entity 'miR-9'

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