PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17214638-4 2007 However, little is known about the correlation between PAI-1 and cyclosporin A-induced gingival overgrowth. Cyclosporine 65-78 serpin family E member 1 Homo sapiens 55-60 18703392-3 2008 Cyclosporine A-induced nephrotoxicity is particularly due to the activation of pro-apoptotic genes leading to tubular atrophy with tubular cell apoptosis and to hemodynamic changes inducing interstitial fibrosis by the activation of factors stimulating the fibroblast proliferation (TGFbeta, Endothelin-A and Plasminogen activator inhibitor-1). Cyclosporine 0-14 serpin family E member 1 Homo sapiens 292-342 25618585-9 2015 Hypoxia increased CsA-induced PAI-1 protein expression than normoxic conditions (p < 0.05). Cyclosporine 18-21 serpin family E member 1 Homo sapiens 30-35 17214638-5 2007 The aim of this study was to investigate the effects of cyclosporin A on the expression of PAI-1 mRNA and protein in human gingival fibroblasts human gingival fibroblasts in vitro and to compare PAI-1 expression in normal healthy gingival tissues and cyclosporin A-induced gingival overgrowth specimens in vivo. Cyclosporine 56-69 serpin family E member 1 Homo sapiens 91-96 17214638-5 2007 The aim of this study was to investigate the effects of cyclosporin A on the expression of PAI-1 mRNA and protein in human gingival fibroblasts human gingival fibroblasts in vitro and to compare PAI-1 expression in normal healthy gingival tissues and cyclosporin A-induced gingival overgrowth specimens in vivo. Cyclosporine 251-264 serpin family E member 1 Homo sapiens 91-96 17214638-8 2007 RESULTS: Investigations of the time dependence of PAI-1 mRNA expression in human gingival fibroblasts treated with 200 ng/ml of cyclosporin A revealed a rapid accumulation of the transcript: a significant signal was first detectable after 1 h of exposure and the signal remained elevated throughout the 24-h incubation period (p < 0.05). Cyclosporine 128-141 serpin family E member 1 Homo sapiens 50-55 17214638-9 2007 Cyclosporin A was also found to up-regulate PAI-1 protein in a time-dependent manner (p < 0.05). Cyclosporine 0-13 serpin family E member 1 Homo sapiens 44-49 17214638-10 2007 The PAI-1 staining in gingival tissue was stronger in the cyclosporin A-induced gingival overgrowth group than in the normal gingival group (p < 0.05). Cyclosporine 58-71 serpin family E member 1 Homo sapiens 4-9 17214638-11 2007 In the cyclosporin A-induced gingival overgrowth group, intensive staining for PAI-1 expression was observed mainly in the cytoplasm of fibroblasts, endothelial cells and inflammatory cells. Cyclosporine 7-20 serpin family E member 1 Homo sapiens 79-84 17214638-12 2007 CONCLUSION: These findings suggest that the up-regulation of PAI-1 may play an important part in the molecular pathogenesis of cyclosporin A-induced gingival overgrowth. Cyclosporine 127-140 serpin family E member 1 Homo sapiens 61-66 17175314-1 2006 We previously confirmed that losartan (LOS), an angiotensin-II (A-II) receptor blocker, diminished plasminogen activator inhibitor-1 (PAI-1) in cyclosporine (CsA)-treated renal graft recipients. Cyclosporine 144-156 serpin family E member 1 Homo sapiens 134-139 17175314-1 2006 We previously confirmed that losartan (LOS), an angiotensin-II (A-II) receptor blocker, diminished plasminogen activator inhibitor-1 (PAI-1) in cyclosporine (CsA)-treated renal graft recipients. Cyclosporine 158-161 serpin family E member 1 Homo sapiens 134-139 12868191-7 2003 RESULTS: In children treated with cyclosporine A increased concentrations of t-PA and PAI-1 were found (p < 0.01). Cyclosporine 34-48 serpin family E member 1 Homo sapiens 86-91 16002416-10 2005 We found that PAI-1 4G allele was associated with progression to renal failure in the group of CsA-treated patients. Cyclosporine 95-98 serpin family E member 1 Homo sapiens 14-19 15848601-0 2005 Inhibition of plasminogen activator inhibitor-1 by angiotensin II receptor blockers on cyclosporine-treated renal allograft recipients. Cyclosporine 87-99 serpin family E member 1 Homo sapiens 14-47 15848601-2 2005 To further evaluate the mechanism, we performed another clinical study focusing on the change in plasma plasminogen activator inhibitor-1 (PAI-1) levels among cyclosporine (CyA)-treated renal allograft recipients. Cyclosporine 159-171 serpin family E member 1 Homo sapiens 104-137 15848601-2 2005 To further evaluate the mechanism, we performed another clinical study focusing on the change in plasma plasminogen activator inhibitor-1 (PAI-1) levels among cyclosporine (CyA)-treated renal allograft recipients. Cyclosporine 159-171 serpin family E member 1 Homo sapiens 139-144 15848601-2 2005 To further evaluate the mechanism, we performed another clinical study focusing on the change in plasma plasminogen activator inhibitor-1 (PAI-1) levels among cyclosporine (CyA)-treated renal allograft recipients. Cyclosporine 173-176 serpin family E member 1 Homo sapiens 104-137 15848601-2 2005 To further evaluate the mechanism, we performed another clinical study focusing on the change in plasma plasminogen activator inhibitor-1 (PAI-1) levels among cyclosporine (CyA)-treated renal allograft recipients. Cyclosporine 173-176 serpin family E member 1 Homo sapiens 139-144 12868191-10 2003 CONCLUSION: Children with remission of idiopathic nephrotic syndrome treated with cyclosporine A show increased concentration of t-PA and PAI-1 and thrombinogenesis. Cyclosporine 82-96 serpin family E member 1 Homo sapiens 138-143 12221903-18 2002 The results of our study suggest a stimulatory effect of CsA on tPA and PAI-I plasma activities as well as on uPA-Ant concentration, while prednisone in turn seems to enhance PAI-I activity in plasma and decrease uPA expression. Cyclosporine 57-60 serpin family E member 1 Homo sapiens 72-75 12221903-18 2002 The results of our study suggest a stimulatory effect of CsA on tPA and PAI-I plasma activities as well as on uPA-Ant concentration, while prednisone in turn seems to enhance PAI-I activity in plasma and decrease uPA expression. Cyclosporine 57-60 serpin family E member 1 Homo sapiens 175-178 10975829-8 2000 Cyclosporin down-regulated the expression of the PAI-1 gene. Cyclosporine 0-11 serpin family E member 1 Homo sapiens 49-54 8671791-8 1996 Hypofibrinolysis induced by elevated PAI levels and increased LDL cholesterol may contribute to the increased thrombogenicity and accelerated atherosclerosis observed in cyclosporin-treated patients. Cyclosporine 170-181 serpin family E member 1 Homo sapiens 37-40 8671791-0 1996 Elevated plasminogen activator inhibitor levels in cyclosporin-treated renal allograft recipients. Cyclosporine 51-62 serpin family E member 1 Homo sapiens 9-40 8671791-4 1996 The plasminogen activator inhibitor (PAI) activity in plasma was clearly increased in CsA-treated patients: 14.5+/-8.8 vs 7.2+/-3.2 in normal controls and 8.5+/-2.4 AU/ml in patients without CsA. Cyclosporine 86-89 serpin family E member 1 Homo sapiens 4-35 8671791-4 1996 The plasminogen activator inhibitor (PAI) activity in plasma was clearly increased in CsA-treated patients: 14.5+/-8.8 vs 7.2+/-3.2 in normal controls and 8.5+/-2.4 AU/ml in patients without CsA. Cyclosporine 86-89 serpin family E member 1 Homo sapiens 37-40 8671791-4 1996 The plasminogen activator inhibitor (PAI) activity in plasma was clearly increased in CsA-treated patients: 14.5+/-8.8 vs 7.2+/-3.2 in normal controls and 8.5+/-2.4 AU/ml in patients without CsA. Cyclosporine 191-194 serpin family E member 1 Homo sapiens 4-35 8671791-4 1996 The plasminogen activator inhibitor (PAI) activity in plasma was clearly increased in CsA-treated patients: 14.5+/-8.8 vs 7.2+/-3.2 in normal controls and 8.5+/-2.4 AU/ml in patients without CsA. Cyclosporine 191-194 serpin family E member 1 Homo sapiens 37-40 8671791-7 1996 Hypercholesterolaemia, obesity, and steroid-induced diabetes could be identified as risk factors for elevated plasma PAI activity in CsA-treated patients. Cyclosporine 133-136 serpin family E member 1 Homo sapiens 117-120 8589211-9 1995 CSA 1 microgram/ml and dexamethasone 1 microgram/ml together were additive in reducing PGI2 release and increasing PAI-1 secretion. Cyclosporine 0-3 serpin family E member 1 Homo sapiens 115-120