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PubMed:15201277 JSONTXT 22 Projects

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Id Subject Object Predicate Lexical cue
T1 0-155 Sentence denotes Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun.
T2 156-286 Sentence denotes Tissue factor is critically important for initiating the activation of coagulation zymogens leading to the generation of thrombin.
T3 287-460 Sentence denotes Quiescent endothelial cells do not express tissue factor on their surface, but many stimuli including cytokines and coagulation proteases can elicit tissue factor synthesis.
T4 461-765 Sentence denotes We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin.
T5 766-860 Sentence denotes We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha.
T6 861-941 Sentence denotes This was due to altered regulation of the transcription factors c-Jun and c-Fos.
T7 942-1055 Sentence denotes The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone.
T8 1056-1167 Sentence denotes Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha.
T9 1168-1305 Sentence denotes These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter.
T10 1306-1526 Sentence denotes Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha.
T11 1527-1784 Sentence denotes Thus, concurrent exposure of vascular endothelial cells to cytokines and procoagulant proteases such as thrombin can result in greatly enhanced tissue factor expression on the endothelium, thereby perpetuating the prothrombotic phenotype of the endothelium.