Results

RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/31111864http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31111864http://www.w3.org/2000/01/rdf-schema#comment"

Background

Atherosclerosis is a chronic inflammatory disease triggered by endothelial dysfunction and exaggerated by macrophage infiltration. Although endothelin-1 (ET-1) plays an important role in vascular inflammation and reactive oxygen species production, the individual effect of ET-1 in atherogenesis remains unclear.

Methods and results

ET-1 expression was increased in mouse atherosclerotic plaques and human umbilical vein endothelial cells (HUVECs) administrated by oxidized low-density lipoprotein stimulation. Moreover, the immunofluorescence co-staining showed upregulated ET-1 expression in endothelial cells. Real-time polymerase chain reaction demonstrated that ET-1 overexpression promoted adhesion molecules and chemokines secretion in HUVECs. Following this intervention, the migration of macrophages and the pro-inflammatory cytokines were increased. More importantly, the endothelial dysfunction regulated by ET-1 and subsequently the effect on macrophage activation were mediated by ETA receptor and largely reversed by protein kinase C (PKC) inhibitor. Eight-week-old male ApoE-/- mice and eET-1/ApoE-/-mice were fed with high-fat diet for 12 weeks. eET-1/ApoE-/-significantly increased atherosclerotic lesions in the whole aorta and aortic sinus, which accompanied by the induction of inflammatory cytokines and macrophages infiltration.

Conclusions

ET-1 accelerates atherogenesis by promoting adhesion molecules and chemokines, as well as subsequent macrophage activation. Collected, these evidence suggest that ET-1 might be a potential target for the treatment of atherogenesis."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.org/dc/terms/identifier"doi:10.1093/ajh/hpz069"xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/author"Xu L."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/author"Wang Y.J."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/author"Zhao W.S."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/author"Yang X.C."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/name"Am J Hypertens"xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/pages"880-889"xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/title"PKC-Mediated Endothelin-1 Expression in Endothelial Cell Promotes Macrophage Activation in Atherogenesis."xsd:string
http://purl.uniprot.org/citations/31111864http://purl.uniprot.org/core/volume"32"xsd:string
http://purl.uniprot.org/citations/31111864http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31111864
http://purl.uniprot.org/citations/31111864http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31111864
http://purl.uniprot.org/uniprot/#_P05305-mappedCitation-31111864http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31111864
http://purl.uniprot.org/uniprot/#_Q6FH53-mappedCitation-31111864http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31111864
http://purl.uniprot.org/uniprot/P05305http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31111864
http://purl.uniprot.org/uniprot/Q6FH53http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31111864