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http://purl.uniprot.org/citations/36963487http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36963487http://www.w3.org/2000/01/rdf-schema#comment"Open-heart surgery is associated with high morbidity, with acute kidney injury (AKI) being one of the most commonly observed postoperative complications. Following open-heart surgery, in an observational study we found significantly higher numbers of blood neutrophils in a group of 13 patients with AKI compared to 25 patients without AKI (AKI: 12.9±5.4 ×109 cells/L; non-AKI: 10.1±2. 9 ×109 cells/L). Elevated serum levels of neutrophil extracellular trap (NETs) components, such as dsDNA, histone 3, and DNA binding protein Y-box protein (YB)-1, were found within the first 24 hours in patients who later developed AKI. We could demonstrate that NET formation and hypoxia triggered the release of YB-1, which was subsequently shown to act as a mediator of kidney tubular damage. Experimentally, in two models of AKI mimicking kidney hypoperfusion during cardiac surgery (bilateral ischemia/reperfusion (I/R) and systemic lipopolysaccharide (LPS) administration), a neutralizing YB-1 antibody was administered to mice. In both models, prophylactic YB-1 antibody administration significantly reduced the tubular damage (damage score range 1-4, the LPS model: non-specific IgG control, 0.92±0.23; anti-YB-1 0.65±0.18; and in the I/R model: non-specific IgG control 2.42±0.23; anti-YB-1 1.86±0.44). Even in a therapeutic, delayed treatment model, antagonism of YB-1 ameliorated AKI (damage score, non-specific IgG control 3.03±0.31; anti-YB-1 2.58±0.18). Thus, blocking extracellular YB-1 reduced the effects induced by hypoxia and NET formation in the kidney and significantly limited AKI, suggesting that YB-1 is part of the NET formation process and an integral mediator of cross-organ effects."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.org/dc/terms/identifier"doi:10.1016/j.kint.2023.02.032"xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Fang Y."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Gao Y."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Gu Y."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Shi Y."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Zhao S."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Ding X."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Song N."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Cai J."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Jankowski V."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Ostendorf T."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Raffetseder U."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Floege J."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Reiss L.K."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Was N."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/author"Leitz A."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/name"Kidney Int"xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/pages"124-138"xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/title"DNA binding protein YB-1 is a part of the neutrophil extracellular trap mediation of kidney damage and cross-organ effects."xsd:string
http://purl.uniprot.org/citations/36963487http://purl.uniprot.org/core/volume"104"xsd:string