PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9402154-9 1997 These results suggest that upregulation of ICAM-1, VCAM-1, and E selectin expression is associated with oxidative stress induced by hemoglobin/heme and that HO-1 may play a modulating role via its ability to degrade heme to a substance with antioxidant properties. Heme 216-220 selectin E Homo sapiens 63-73 9402154-0 1997 Heme induces the expression of adhesion molecules ICAM-1, VCAM-1, and E selectin in vascular endothelial cells. Heme 0-4 intercellular adhesion molecule 1 Homo sapiens 50-56 9402154-0 1997 Heme induces the expression of adhesion molecules ICAM-1, VCAM-1, and E selectin in vascular endothelial cells. Heme 0-4 vascular cell adhesion molecule 1 Homo sapiens 58-64 9402154-0 1997 Heme induces the expression of adhesion molecules ICAM-1, VCAM-1, and E selectin in vascular endothelial cells. Heme 0-4 selectin E Homo sapiens 70-80 9402154-2 1997 To investigate the mechanism of heme-induced endothelial cell activation, we analyzed the effect of heme and the inflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), on the expression of the heme-degrading stress protein, heme oxygenase (HO), and adhesion molecules in human umbilical vein endothelial cells (HUVEC). Heme 32-36 tumor necrosis factor Homo sapiens 165-174 9402154-3 1997 Indirect immunofluorescence double labeling studies demonstrated a simultaneous increase of ICAM-1 and HO-1 after exposure of cells to heme for 24 hr. Heme 135-139 intercellular adhesion molecule 1 Homo sapiens 92-98 9402154-3 1997 Indirect immunofluorescence double labeling studies demonstrated a simultaneous increase of ICAM-1 and HO-1 after exposure of cells to heme for 24 hr. Heme 135-139 heme oxygenase 1 Homo sapiens 103-107 9402154-5 1997 Dot blot immunoassay and quantitative analysis by ELISA demonstrated that heme treatment for 24 hr caused a 2-fold increase in ICAM-1 expression (P < 0.002) compared with quiescent cells, while in cells stimulated by TNF-alpha for 24 hr ICAM-1 gene expression increased by 5-fold. Heme 74-78 intercellular adhesion molecule 1 Homo sapiens 127-133 9402154-5 1997 Dot blot immunoassay and quantitative analysis by ELISA demonstrated that heme treatment for 24 hr caused a 2-fold increase in ICAM-1 expression (P < 0.002) compared with quiescent cells, while in cells stimulated by TNF-alpha for 24 hr ICAM-1 gene expression increased by 5-fold. Heme 74-78 tumor necrosis factor Homo sapiens 220-229 9402154-5 1997 Dot blot immunoassay and quantitative analysis by ELISA demonstrated that heme treatment for 24 hr caused a 2-fold increase in ICAM-1 expression (P < 0.002) compared with quiescent cells, while in cells stimulated by TNF-alpha for 24 hr ICAM-1 gene expression increased by 5-fold. Heme 74-78 intercellular adhesion molecule 1 Homo sapiens 240-246 9402154-6 1997 Moreover, heme exposure also resulted in a marked increase in VCAM-1 and E selectin expression (three and four times over control levels, respectively). Heme 10-14 vascular cell adhesion molecule 1 Homo sapiens 62-68 9402154-6 1997 Moreover, heme exposure also resulted in a marked increase in VCAM-1 and E selectin expression (three and four times over control levels, respectively). Heme 10-14 selectin E Homo sapiens 73-83 9402154-8 1997 The level of HO activity in endothelial cells exposed to heme or TNF-alpha was increased from 24.7 +/- 5.7 pmol bilirubin/mg protein/min in control to 70.0 +/- 9.5 and 36.7 +/- 3.1 pmol bilirubin/mg protein/min in heme- and TNF-alpha-stimulated cells, respectively. Heme 57-61 tumor necrosis factor Homo sapiens 224-233 9402154-8 1997 The level of HO activity in endothelial cells exposed to heme or TNF-alpha was increased from 24.7 +/- 5.7 pmol bilirubin/mg protein/min in control to 70.0 +/- 9.5 and 36.7 +/- 3.1 pmol bilirubin/mg protein/min in heme- and TNF-alpha-stimulated cells, respectively. Bilirubin 112-121 tumor necrosis factor Homo sapiens 65-74 9402154-8 1997 The level of HO activity in endothelial cells exposed to heme or TNF-alpha was increased from 24.7 +/- 5.7 pmol bilirubin/mg protein/min in control to 70.0 +/- 9.5 and 36.7 +/- 3.1 pmol bilirubin/mg protein/min in heme- and TNF-alpha-stimulated cells, respectively. Bilirubin 186-195 tumor necrosis factor Homo sapiens 65-74 9402154-8 1997 The level of HO activity in endothelial cells exposed to heme or TNF-alpha was increased from 24.7 +/- 5.7 pmol bilirubin/mg protein/min in control to 70.0 +/- 9.5 and 36.7 +/- 3.1 pmol bilirubin/mg protein/min in heme- and TNF-alpha-stimulated cells, respectively. Heme 214-218 tumor necrosis factor Homo sapiens 65-74 9402154-9 1997 These results suggest that upregulation of ICAM-1, VCAM-1, and E selectin expression is associated with oxidative stress induced by hemoglobin/heme and that HO-1 may play a modulating role via its ability to degrade heme to a substance with antioxidant properties. Heme 143-147 intercellular adhesion molecule 1 Homo sapiens 43-49 9402154-9 1997 These results suggest that upregulation of ICAM-1, VCAM-1, and E selectin expression is associated with oxidative stress induced by hemoglobin/heme and that HO-1 may play a modulating role via its ability to degrade heme to a substance with antioxidant properties. Heme 143-147 vascular cell adhesion molecule 1 Homo sapiens 51-57 9402154-9 1997 These results suggest that upregulation of ICAM-1, VCAM-1, and E selectin expression is associated with oxidative stress induced by hemoglobin/heme and that HO-1 may play a modulating role via its ability to degrade heme to a substance with antioxidant properties. Heme 143-147 selectin E Homo sapiens 63-73 9402154-9 1997 These results suggest that upregulation of ICAM-1, VCAM-1, and E selectin expression is associated with oxidative stress induced by hemoglobin/heme and that HO-1 may play a modulating role via its ability to degrade heme to a substance with antioxidant properties. Heme 216-220 intercellular adhesion molecule 1 Homo sapiens 43-49 9402154-9 1997 These results suggest that upregulation of ICAM-1, VCAM-1, and E selectin expression is associated with oxidative stress induced by hemoglobin/heme and that HO-1 may play a modulating role via its ability to degrade heme to a substance with antioxidant properties. Heme 216-220 heme oxygenase 1 Homo sapiens 157-161