PubMed:7940740 JSONTXT

{"project":"Wangshuguang","denotations":[{"id":"T1","span":{"begin":172,"end":180},"obj":"B-Variation"},{"id":"T2","span":{"begin":250,"end":258},"obj":"B-Variation"},{"id":"T3","span":{"begin":259,"end":270},"obj":"I-Variation"},{"id":"T4","span":{"begin":271,"end":280},"obj":"I-Variation"},{"id":"T5","span":{"begin":331,"end":339},"obj":"B-Variation"},{"id":"T6","span":{"begin":742,"end":751},"obj":"B-Regulation"},{"id":"T7","span":{"begin":752,"end":754},"obj":"I-Regulation"},{"id":"T8","span":{"begin":759,"end":766},"obj":"B-Variation"},{"id":"T9","span":{"begin":935,"end":944},"obj":"B-Regulation"},{"id":"T10","span":{"begin":945,"end":947},"obj":"I-Regulation"},{"id":"T11","span":{"begin":952,"end":963},"obj":"B-Negative_Function"},{"id":"T12","span":{"begin":1180,"end":1190},"obj":"B-Cell_Physiological_Activity"},{"id":"T13","span":{"begin":1191,"end":1201},"obj":"I-Cell_Physiological_Activity"},{"id":"T14","span":{"begin":1369,"end":1379},"obj":"B-Molecular_Activity"},{"id":"T15","span":{"begin":1384,"end":1391},"obj":"B-Positive_Regulation"},{"id":"T1","span":{"begin":172,"end":180},"obj":"B-Variation"},{"id":"T2","span":{"begin":250,"end":258},"obj":"B-Variation"},{"id":"T3","span":{"begin":259,"end":270},"obj":"I-Variation"},{"id":"T4","span":{"begin":271,"end":280},"obj":"I-Variation"},{"id":"T5","span":{"begin":331,"end":339},"obj":"B-Variation"},{"id":"T6","span":{"begin":742,"end":751},"obj":"B-Regulation"},{"id":"T7","span":{"begin":752,"end":754},"obj":"I-Regulation"},{"id":"T8","span":{"begin":759,"end":766},"obj":"B-Variation"},{"id":"T9","span":{"begin":935,"end":944},"obj":"B-Regulation"},{"id":"T10","span":{"begin":945,"end":947},"obj":"I-Regulation"},{"id":"T11","span":{"begin":952,"end":963},"obj":"B-Negative_Function"},{"id":"T12","span":{"begin":1180,"end":1190},"obj":"B-Cell_Physiological_Activity"},{"id":"T13","span":{"begin":1191,"end":1201},"obj":"I-Cell_Physiological_Activity"},{"id":"T14","span":{"begin":1369,"end":1379},"obj":"B-Molecular_Activity"},{"id":"T15","span":{"begin":1384,"end":1391},"obj":"B-Positive_Regulation"}],"text":"Phenotypic variations in resting and activated levels of ICAM-1 expression by cultured human aortic endothelial cells.\nICAM-1 is an inducible glycoprotein important in the adhesion, activation, and transmigration of circulating leukocytes across the vascular endothelial monolayer, and it likely plays a key role in the allogeneic response. To determine the reproducibility and significance of variations in resting levels of cell surface ICAM-1, 3 individual measurements of ICAM-1 levels were performed on 26 individual isolates of human aortic endothelial cells (HAECs) both at rest and following activation by allogeneic lymphocytes, using flow cytometry. Resting HAEC ICAM-1 levels varied 10-fold (range 6-60 mean fluorescence channels) depending on the isolate studied. There were strong correlations (r = 0.71 to 0.77, P \u003c 0.0001) between the three measurements (performed no closer than weekly intervals on separate cultures), attesting to the consistency of the phenotypic expression. Constitutive expression of ICAM-1 was not affected by cell age, based upon comparing a subset of these isolates across 3 population doublings. Levels of HAEC ICAM-1 following allogeneic lymphocyte activation varied 15-fold (range 20-300 mean fluorescent channels) and, more important, correlated with resting ICAM-1 levels (r = 0.58, P = 0.002). Finally, constitutive ICAM-1 expression was related to TNF-alpha-induced ICAM-1 levels based upon a subset of the isolates studied. These data suggest that phenotypic, and likely genetic, differences in quiescent endothelial cell adhesion molecule expression can influence inflammatory responses including alloresponsiveness to the vasculature."}

{"project":"123123123","denotations":[{"id":"T1","span":{"begin":172,"end":180},"obj":"B-Variation"},{"id":"T2","span":{"begin":250,"end":258},"obj":"B-Variation"},{"id":"T3","span":{"begin":259,"end":270},"obj":"I-Variation"},{"id":"T4","span":{"begin":271,"end":280},"obj":"I-Variation"},{"id":"T5","span":{"begin":331,"end":339},"obj":"B-Variation"},{"id":"T6","span":{"begin":742,"end":751},"obj":"B-Regulation"},{"id":"T7","span":{"begin":752,"end":754},"obj":"I-Regulation"},{"id":"T8","span":{"begin":759,"end":766},"obj":"B-Variation"},{"id":"T9","span":{"begin":935,"end":944},"obj":"B-Regulation"},{"id":"T10","span":{"begin":945,"end":947},"obj":"I-Regulation"},{"id":"T11","span":{"begin":952,"end":963},"obj":"B-Negative_Function"},{"id":"T12","span":{"begin":1180,"end":1190},"obj":"B-Cell_Physiological_Activity"},{"id":"T13","span":{"begin":1191,"end":1201},"obj":"I-Cell_Physiological_Activity"},{"id":"T14","span":{"begin":1369,"end":1379},"obj":"B-Molecular_Activity"},{"id":"T15","span":{"begin":1384,"end":1391},"obj":"B-Positive_Regulation"}],"text":"Phenotypic variations in resting and activated levels of ICAM-1 expression by cultured human aortic endothelial cells.\nICAM-1 is an inducible glycoprotein important in the adhesion, activation, and transmigration of circulating leukocytes across the vascular endothelial monolayer, and it likely plays a key role in the allogeneic response. To determine the reproducibility and significance of variations in resting levels of cell surface ICAM-1, 3 individual measurements of ICAM-1 levels were performed on 26 individual isolates of human aortic endothelial cells (HAECs) both at rest and following activation by allogeneic lymphocytes, using flow cytometry. Resting HAEC ICAM-1 levels varied 10-fold (range 6-60 mean fluorescence channels) depending on the isolate studied. There were strong correlations (r = 0.71 to 0.77, P \u003c 0.0001) between the three measurements (performed no closer than weekly intervals on separate cultures), attesting to the consistency of the phenotypic expression. Constitutive expression of ICAM-1 was not affected by cell age, based upon comparing a subset of these isolates across 3 population doublings. Levels of HAEC ICAM-1 following allogeneic lymphocyte activation varied 15-fold (range 20-300 mean fluorescent channels) and, more important, correlated with resting ICAM-1 levels (r = 0.58, P = 0.002). Finally, constitutive ICAM-1 expression was related to TNF-alpha-induced ICAM-1 levels based upon a subset of the isolates studied. These data suggest that phenotypic, and likely genetic, differences in quiescent endothelial cell adhesion molecule expression can influence inflammatory responses including alloresponsiveness to the vasculature."}