| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-113 |
Sentence |
denotes |
Regulation of lung endothelial permeability and inflammatory responses by prostaglandin A2: role of EP4 receptor. |
| T2 |
114-208 |
Sentence |
denotes |
The role of prostaglandin A2 (PGA2) in modulation of vascular endothelial function is unknown. |
| T3 |
209-367 |
Sentence |
denotes |
We investigated effects of PGA2 on pulmonary endothelial cell (EC) permeability and inflammatory activation and identified a receptor mediating these effects. |
| T4 |
368-537 |
Sentence |
denotes |
PGA2 enhanced the EC barrier and protected against barrier dysfunction caused by vasoactive peptide thrombin and proinflammatory bacterial wall lipopolysaccharide (LPS). |
| T5 |
538-655 |
Sentence |
denotes |
Receptor screening using pharmacological and molecular inhibitory approaches identified EP4 as a novel PGA2 receptor. |
| T6 |
656-853 |
Sentence |
denotes |
EP4 mediated barrier-protective effects of PGA2 by activating Rap1/Rac1 GTPase and protein kinase A targets at cell adhesions and cytoskeleton: VE-cadherin, p120-catenin, ZO-1, cortactin, and VASP. |
| T7 |
854-997 |
Sentence |
denotes |
PGA2 also suppressed LPS-induced inflammatory signaling by inhibiting the NFκB pathway and expression of EC adhesion molecules ICAM1 and VCAM1. |
| T8 |
998-1077 |
Sentence |
denotes |
These effects were abolished by pharmacological or molecular inhibition of EP4. |
| T9 |
1078-1304 |
Sentence |
denotes |
In vivo, PGA2 was protective in two distinct models of acute lung injury (ALI): LPS-induced inflammatory injury and two-hit ALI caused by suboptimal mechanical ventilation and injection of thrombin receptor-activating peptide. |
| T10 |
1305-1392 |
Sentence |
denotes |
These protective effects were abolished in mice with endothelial-specific EP4 knockout. |
| T11 |
1393-1590 |
Sentence |
denotes |
The results suggest a novel role for the PGA2-EP4 axis in vascular EC protection that is critical for improvement of pathological states associated with increased vascular leakage and inflammation. |