About: Autophagic response in the Rabbit Hemorrhagic Disease, an animal model of virally-induced fulminant hepatic failure

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About: Autophagic response in the Rabbit Hemorrhagic Disease, an animal model of virally-induced fulminant hepatic failure 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	Autophagic response in the Rabbit Hemorrhagic Disease, an animal model of virally-induced fulminant hepatic failure
Creator	Crespo, Irene González-Gallego, Javier Prieto, Jesús San-Miguel, Beatriz Vallejo, Daniela Tuñón, María
topic	covid:1c995ac4ae70bbcc5da53211e20df4398d1ce55d#this
Source	Medline; PMC
abstract	The Rabbit Hemorrhagic Disease Virus (RHDV) induces a severe disease that fulfils many requirements of an animal model of fulminant hepatic failure. However, a better knowledge of molecular mechanisms contributing to liver damage is required, and it is unknown whether the RHDV induces liver autophagy and how it relates to apoptosis. In this study, we attempted to explore which signalling pathways were involved in the autophagic response induced by the RHDV and to characterize their role in the context of RHDV pathogenesis. Rabbits were infected with 2 × 10(4) hemmaglutination units of a RHDV isolate. The autophagic response was measured as presence of autophagic vesicles, LC3 staining, conversion of LC3-I to autophagosome-associated LC3-II and changes in expression of beclin-1, UVRAG, Atg5, Atg12, Atg16L1 and p62/SQSTM1. RHDV-triggered autophagy reached a maximum at 24 hours post-infection (hpi) and declined at 30 and 36 hpi. Phosphorylation of mTOR also augmented in early periods of infection and there was an increase in the expression of the endoplasmic reticulum chaperones BiP/GRP78, CHOP and GRP94. Apoptosis, measured as caspase-3 activity and expression of PARP-1, increased significantly at 30 and 36 hpi in parallel to the maximal expression of the RHDV capsid protein VP60. These data indicate that RHDV infection initiates a rapid autophagic response, perhaps in an attempt to protect liver, which associates to ER stress development and is independent from downregulation of the major autophagy suppressor mTOR. As the infection continues and the autophagic response declines, cells begin to exhibit apoptosis.
has issue date	2014-02-04(xsd:dateTime)
bibo:doi	10.1186/1297-9716-45-15
bibo:pmid	24490870
has license	cc-by
sha1sum (hex)	1c995ac4ae70bbcc5da53211e20df4398d1ce55d
schema:url	https://doi.org/10.1186/1297-9716-45-15
resource representing a document's title	Autophagic response in the Rabbit Hemorrhagic Disease, an animal model of virally-induced fulminant hepatic failure
has PubMed Central identifier	PMC3922607
has PubMed identifier	24490870
schema:publication	Vet Res
resource representing a document's body	covid:1c995ac4ae70bbcc5da53211e20df4398d1ce55d#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/1c995ac4ae70bbcc5da53211e20df4398d1ce55d https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/1c995ac4ae70bbcc5da53211e20df4398d1ce55d
is schema:about of	named entity 'AUTOPHAGY' named entity 'ANIMAL MODEL' named entity 'RABBIT HEMORRHAGIC DISEASE VIRUS' named entity 'ENDOPLASMIC RETICULUM' named entity 'RELATES' named entity 'PATHWAYS' named entity 'INDEPENDENT' named entity 'P62' named entity 'MAJOR' named entity 'RABBITS' named entity 'MOLECULAR' named entity 'BIP' named entity 'THESE' named entity 'ATTEMPTED' named entity 'GRP94' named entity 'RAPID' named entity 'POST' named entity 'MTOR' named entity 'LIVER DAMAGE' named entity 'SUPPRESSOR' named entity 'REQUIRED' named entity 'PATHOGENESIS' named entity 'MEASURED' named entity 'PARP-1' named entity 'ROLE' named entity 'response' named entity 'Apoptosis' named entity 'caspase' named entity 'autophagic' named entity 'declines' named entity 'mTOR' named entity 'pathogenesis' named entity 'Rabbit' covid:arg/1c995ac4ae70bbcc5da53211e20df4398d1ce55d named entity 'INDUCED' named entity 'MAXIMAL' named entity 'RESPONSE' named entity 'INVOLVED' named entity 'EXPRESSION' named entity 'INCREASE' named entity 'AUTOPHAGOSOME' named entity 'TO CHARACTERIZE' named entity 'CHOP' named entity 'PROTEIN ' named entity 'HPI' named entity 'THEIR' named entity 'DATA' named entity 'KNOWLEDGE' named entity 'UVRAG' named entity 'CONVERSION' named entity 'CHANGES' named entity 'APOPTOSIS' named entity 'ER STRESS' named entity 'ATTEMPT' named entity 'ANIMAL MODEL' named entity 'RESPONSE' named entity 'RABBIT' named entity 'INFECTED' named entity 'LIVER' named entity 'INFECTION' named entity 'UNITS' named entity 'MAXIMUM' named entity 'PARALLEL TO' named entity '24 HOURS' named entity 'CASPASE-3 ACTIVITY' named entity 'CONTRIBUTING' named entity 'DEVELOPMENT' named entity 'TRIGGERED' named entity 'LC3-II' named entity 'BECLIN-1' named entity 'AUGMENTED' named entity 'FULMINANT HEPATIC FAILURE' named entity 'REQUIREMENTS'

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