PMC:7373848 / 22454-23289 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7373848","sourcedb":"PMC","sourceid":"7373848","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7373848","text":"Neutrophil activation causes endothelial cell injury\nNeutrophil activation and neutrophil extracellular traps (NETs) cause endothelial cell glycocalyx injury [49]. The concentration of circulating histones is directly proportional to the degree of inflammation and end organ dysfunction in trauma or sepsis-like conditions. Exposure of endothelial cells to histones causes decreased vasodilation and cell death in 25% of cells [50]. Citrullinated histones 3 (H3CiT) can directly contribute to NET-associated inflammatory responses and opens cell–cell adherans junctions impairing vascular integrity [51]. The bioactive proteins released from NETs that cause tissue injury include myeloperoxidase (MPO), neutrophil elastase (NE), matrix metalloproteinase (MMP)-9, high-mobility group box (HMGB)-1, proteinase (PTN)-3 and properdin 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