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PubMed:26269588 JSONTXT 22 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T1 0-86 Sentence denotes Neutrophil elastase promotes interleukin-1β secretion from human coronary endothelium.
T2 87-222 Sentence denotes The endothelium is critically involved in the pathogenesis of atherosclerosis by producing pro-inflammatory mediators, including IL-1β.
T3 223-333 Sentence denotes Coronary arteries from patients with ischemic heart disease express large amounts of IL-1β in the endothelium.
T4 334-429 Sentence denotes However, the mechanism by which endothelial cells (ECs) release IL-1β remains to be elucidated.
T5 430-610 Sentence denotes We investigated neutrophil elastase (NE), a potent serine protease detected in vulnerable areas of human carotid plaques, as a potential "trigger" for IL-1β processing and release.
T6 611-732 Sentence denotes This study tested the hypothesis that NE potentiates the processing and release of IL-1β from human coronary endothelium.
T7 733-869 Sentence denotes We found that NE cleaves the pro-isoform of IL-1β in ECs and causes significant secretion of bioactive IL-1β via extracellular vesicles.
T8 870-967 Sentence denotes This release was attenuated significantly by inhibition of neutrophil elastase but not caspase-1.
T9 968-1052 Sentence denotes Transient increases in intracellular Ca(2+) levels were observed prior to secretion.
T10 1053-1158 Sentence denotes Inside ECs, and after NE treatment only, IL-1β was detected within LAMP-1-positive multivesicular bodies.
T11 1159-1207 Sentence denotes The released vesicles contained bioactive IL-1β.
T12 1208-1351 Sentence denotes In vivo, in experimental atherosclerosis, NE was detected in mature atherosclerotic plaques, predominantly in the endothelium, alongside IL-1β.
T13 1352-1513 Sentence denotes This study reveals a novel mechanistic link between NE expression in atherosclerotic plaques and concomitant pro-inflammatory bioactive IL-1β secretion from ECs.
T14 1514-1678 Sentence denotes This could reveal additional potential anti-IL-1β therapeutic targets and provide further insights into the inflammatory process by which vascular disease develops.