About: Up-regulation of DcR3 in microbial toxins-stimulated HUVECs involves NF-κB signalling

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About: Up-regulation of DcR3 in microbial toxins-stimulated HUVECs involves NF-κB signalling 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	Up-regulation of DcR3 in microbial toxins-stimulated HUVECs involves NF-κB signalling
Creator	Liu, Yang Chen, Hongwei Hou, Yanqiang Liang, Dongyu Lou, Xiaoli
Source	PMC
abstract	BACKGROUND: Sepsis is a severe condition characterised by the body’s systemic inflammatory response to infection. The specific sepsis-related biomarkers should be used in clinical diagnosis, therapeutic response monitoring, rational use of antibiotics, and prognosis (risk stratification), etc. RESULTS: In this study, we investigated the expression level of Decoy Receptor 3 (DcR3) and the mechanism of high expression in sepsis patients. Septic cell model experiments were performed by treating human umbilical vein endothelial cells (HUVECs) and Jurkat cells with lipopolysaccharide (LPS), lipoteichoic acid (LTA) and zymosan, respectively. SP600125, SB203580 and ammonium pyrrolidinedithiocarbamate (PDTC) were used to inhibit JNK1/2, p38MAPK and NF-κB signalling pathways in septic cell model, respectively. These results showed that DcR3 levels were higher in sepsis group than control. DcR3 mRNA and protein levels in HUVECs were increased following treatment with LPS, LTA and zymosan, and also increased in Jurkat cells treated by LPS, but not by LTA or zymosan. When HUVECs were treated with the NF-κB inhibitor PDTC, DcR3 expression was decreased compared with controls. However, SP600125 and SB203580 had no effect on DcR3 mRNA or protein levels. CONCLUSIONS: The results indicated that DcR3 secretion proceeded through the NF-κB signalling pathway in HUVECs.
has issue date	2018-12-27(xsd:dateTime)
bibo:doi	10.1186/s12858-018-0102-z
bibo:pmid	30587127
has license	cc-by
sha1sum (hex)	6bfd2809e31c992d160d33b11111f8cebda23876
schema:url	https://doi.org/10.1186/s12858-018-0102-z
resource representing a document's title	Up-regulation of DcR3 in microbial toxins-stimulated HUVECs involves NF-κB signalling
has PubMed Central identifier	PMC6307204
has PubMed identifier	30587127
schema:publication	BMC Biochem
resource representing a document's body	covid:6bfd2809e31c992d160d33b11111f8cebda23876#body_text
is schema:about of	named entity 'controls' named entity 'LPS' named entity 'endothelial cells' named entity 'Results' named entity 'specific' named entity 'Jurkat cells' named entity 'signalling pathways' named entity 'SEPSIS' named entity 'TREATED' named entity 'PERFORMED BY' named entity 'USE OF' named entity 'DCR3' named entity 'COMPARED' named entity 'INVESTIGATED' named entity 'STUDY' named entity 'TREATING' named entity 'CELL MODEL' named entity 'HIGHER' named entity 'TREATED WITH' named entity 'THESE' named entity 'PDTC' named entity 'CONDITION' named entity 'INFECTION' named entity 'ETC.' named entity 'USED' named entity 'DECREASED' named entity 'SEVERE' named entity 'INCREASED' named entity 'SPECIFIC' named entity 'LIPOTEICHOIC ACID' named entity 'HUVECs' named entity 'HUVECs' named entity 'risk stratification' named entity 'monitoring' named entity 'sepsis' named entity 'protein' named entity 'ammonium' named entity 'response' named entity 'Sepsis' named entity 'zymosan' named entity 'antibiotics' named entity 'sepsis' named entity 'prognosis' named entity 'mRNA' named entity 'SP600125' named entity 'systemic inflammatory response' named entity 'clinical diagnosis' named entity 'DcR3' named entity 'biomarkers' named entity 'SB203580' named entity 'lipopolysaccharide' named entity 'mRNA' named entity 'SB203580' named entity 'NF-κB' named entity 'inflammatory response' named entity 'control group' named entity 'ICU' named entity 'receptor' named entity 'DcR3' named entity 'septic shock' named entity 'sepsis' named entity 'Jurkat cells' named entity 'sepsis' named entity 'antibiotics' named entity 'blood samples' named entity 'DcR3' named entity 'Songjiang District' named entity 'HUVECs' named entity 'HUVECs' named entity 'DcR3' named entity 'DcR3' named entity 'HUVECs' named entity 'microbial' named entity 'inflammatory response' named entity 'biological replicates' named entity 'DcR3' named entity 'DcR3'

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