| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-215 |
Sentence |
denotes |
Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. |
| T2 |
216-326 |
Sentence |
denotes |
Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. |
| T3 |
327-545 |
Sentence |
denotes |
Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells. |
| T4 |
546-650 |
Sentence |
denotes |
VEGF (20 ng/ml) increased expression of ICAM-1, VCAM-1, and E-selectin mRNAs in a time-dependent manner. |
| T5 |
651-1020 |
Sentence |
denotes |
These effects were significantly suppressed by Flk-1/kinase-insert domain containing receptor (KDR) antagonist and by inhibitors of phospholipase C, nuclear factor (NF)-kappaB, sphingosine kinase, and protein kinase C, but they were not affected by inhibitors of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 or nitric-oxide synthase. |
| T6 |
1021-1262 |
Sentence |
denotes |
Unexpectedly, the phosphatidylinositol (PI) 3'-kinase inhibitor wortmannin enhanced both basal and VEGF-stimulated adhesion molecule expression, whereas insulin, a PI 3'-kinase activator, suppressed both basal and VEGF-stimulated expression. |
| T7 |
1263-1331 |
Sentence |
denotes |
Gel shift analysis revealed that VEGF stimulated NF-kappaB activity. |
| T8 |
1332-1419 |
Sentence |
denotes |
This effect was inhibited by phospholipase C, NF-kappaB, or protein kinase C inhibitor. |
| T9 |
1420-1537 |
Sentence |
denotes |
VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. |
| T10 |
1538-1756 |
Sentence |
denotes |
These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activation with PI 3'-kinase-mediated suppression, but was independent of nitric oxide and MEK. |
| T11 |
1757-1904 |
Sentence |
denotes |
Thus, VEGF simultaneously activates two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression. |
| T12 |
1905-2041 |
Sentence |
denotes |
The existence of parallel inverse signaling implies that the induction of adhesion molecule expression by VEGF is very finely regulated. |