About: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells

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About: Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells
Creator	Li, Jun Wang, Nan Sun, Zhixiao Zhang, Mingshun Ma, Qiyun Sun, Jiandong Wang, Wenjing Xu, Juan
Source	Medline; PMC
abstract	Enterovirus A71 (EV-A71) is the major cause of severe hand-foot-and-mouth diseases (HFMD), especially encephalitis and other nervous system diseases. EV-A71 capsid protein VP1 mediates virus attachment and is the important virulence factor in the EV-A71pathogenesis. In this study, we explored the roles of VP1 in the permeability of blood–brain barrier (BBB). Sera albumin, Evans blue, and dextran leaked into brain parenchyma of the 1-week-old C57BL/6J mice intracranially injected with VP1 recombinant protein. VP1 also increased the permeability of the brain endothelial cells monolayer, an in vitro BBB model. Tight junction protein claudin-5 was reduced in the brain tissues or brain endothelial cells treated with VP1. In contrast, VP1 increased the expression of virus receptor vimentin, which could be blocked with VP1 neutralization antibody. Vimentin expression in the VP1-treated brain endothelial cells was regulated by TGF-β/Smad-3 and NF-κB signal pathways. Moreover, vimentin over-expression was accompanied with compromised BBB. From these studies, we conclude that EV-A71 virus capsid protein VP1 disrupted BBB and increased virus receptor vimentin, which both may contribute to the virus entrance into brain and EV-A71 CNS infection.
has issue date	2019-09-11(xsd:dateTime)
bibo:doi	10.1007/s13365-019-00800-8
bibo:pmid	31512144
has license	cc-by
sha1sum (hex)	0a89d01436c87dbd802431eb574ed0dd486d4d6e
schema:url	https://doi.org/10.1007/s13365-019-00800-8
resource representing a document's title	Enterovirus A71 capsid protein VP1 increases blood–brain barrier permeability and virus receptor vimentin on the brain endothelial cells
has PubMed Central identifier	PMC7040057
has PubMed identifier	31512144
schema:publication	J Neurovirol
resource representing a document's body	covid:0a89d01436c87dbd802431eb574ed0dd486d4d6e#body_text
is schema:about of	named entity 'TREATED WITH' named entity 'BRAIN ENDOTHELIAL CELLS' named entity 'C57BL' named entity 'BLOCKED' named entity 'BAB' named entity 'MEDIATES' named entity 'ROLES' named entity 'ENTEROVIRUS A71' named entity 'MAJOR' named entity 'IMPORTANT' named entity 'PERMEABILITY' named entity 'BBB MODEL' named entity 'DEXTRAN' named entity 'CAPSID PROTEIN' named entity 'SERA' named entity 'BLOOD-BRAIN BARRIER' named entity 'CLAUDIN-5' named entity 'IN VITRO' named entity 'SEVERE' named entity 'VIRUS RECEPTOR' named entity 'BRAIN PARENCHYMA' named entity 'STUDY' named entity 'VIRUS' named entity 'CNS INFECTION' named entity 'ENTRANCE' named entity 'ENCEPHALITIS' named entity 'NERVOUS SYSTEM DISEASES' named entity 'TREATED' named entity 'BLOOD-BRAIN BARRIER PERMEABILITY' named entity 'VP1' named entity 'VIRUS RECEPTOR' named entity 'MICE' named entity 'TGF' named entity 'INCREASED' named entity 'CONTRAST' named entity 'PROTEIN ' named entity 'EXPRESSION' named entity 'COULD BE' named entity 'FOOT-AND-MOUTH DISEASES' named entity 'HAND' named entity 'EVANS BLUE' named entity 'RECOMBINANT PROTEIN' named entity 'REDUCED' named entity 'THE BRAIN' named entity 'PROTEIN ' named entity 'ENTEROVIRUS A71' named entity 'VIMENTIN' named entity 'CAPSID PROTEIN' named entity 'BRAIN ENDOTHELIAL CELLS' named entity 'INCREASES' named entity 'THE BRAIN' named entity 'THESE' named entity 'VIRULENCE FACTOR' named entity 'CONTRIBUTE ' named entity 'BRAIN' named entity 'OLD' named entity 'BRAIN TISSUES' named entity 'VIMENTIN' named entity 'ALBUMIN' named entity 'WEEK' named entity 'A71' named entity 'DISRUPTED' named entity 'BBB' named entity 'CONCLUDE' named entity 'STUDIES' named entity 'VIRUS ATTACHMENT' named entity 'ANTIBODY' named entity 'SIGNAL' named entity 'MONOLAYER' named entity 'VP1' named entity 'TIGHT JUNCTION' named entity 'CAUSE' named entity 'REGULATED' named entity 'PATHWAYS'

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