PubMed:12548614
Annnotations
DisGeNET
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T0 | 40-45 | gene:55065 | denotes | PAR-2 |
| T1 | 127-142 | disease:C0001418 | denotes | adenocarcinomas |
| T2 | 40-45 | gene:2150 | denotes | PAR-2 |
| T3 | 127-142 | disease:C0001418 | denotes | adenocarcinomas |
| T4 | 40-45 | gene:8856 | denotes | PAR-2 |
| T5 | 127-142 | disease:C0001418 | denotes | adenocarcinomas |
| R1 | T0 | T1 | associated_with | PAR-2,adenocarcinomas |
| R2 | T2 | T3 | associated_with | PAR-2,adenocarcinomas |
| R3 | T4 | T5 | associated_with | PAR-2,adenocarcinomas |
DisGeNET5_gene_disease
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| 12548614-0#40#45#gene2150 | 40-45 | gene2150 | denotes | PAR-2 |
| 12548614-0#40#45#gene8856 | 40-45 | gene8856 | denotes | PAR-2 |
| 12548614-0#40#45#gene55065 | 40-45 | gene55065 | denotes | PAR-2 |
| 12548614-0#127#142#diseaseC0001418 | 127-142 | diseaseC0001418 | denotes | adenocarcinomas |
| 40#45#gene2150127#142#diseaseC0001418 | 12548614-0#40#45#gene2150 | 12548614-0#127#142#diseaseC0001418 | associated_with | PAR-2,adenocarcinomas |
| 40#45#gene8856127#142#diseaseC0001418 | 12548614-0#40#45#gene8856 | 12548614-0#127#142#diseaseC0001418 | associated_with | PAR-2,adenocarcinomas |
| 40#45#gene55065127#142#diseaseC0001418 | 12548614-0#40#45#gene55065 | 12548614-0#127#142#diseaseC0001418 | associated_with | PAR-2,adenocarcinomas |
PubMed_Structured_Abstracts
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T1 | 156-288 | BACKGROUND | denotes | Cell growth can be induced via elicitation of protease-activated receptors (PAR) with serine proteases such as thrombin and trypsin. |
| T2 | 298-580 | METHODS | denotes | To understand whether PAR are involved in tumor vessel formation in the neoplastic cell-bearing alveolar walls, immunohistochemical and reverse transcriptase-polymerase chain reaction analyses were performed using the lung tissues from 16 patients with primary lung adenocarcinomas. |
| T3 | 590-1649 | RESULTS | denotes | In microdissected tumor alveolar walls, the expressions of PAR-1 and PAR-2 mRNA were increased by 10-fold (P < 0.05) and 16-fold (P < 0.01), respectively, as compared with normal alveolar walls. Confocal microscopy revealed that tumor capillary endothelial cells in alveolar walls lost thrombomodulin expression. Instead, the expression of PAR-2 often became obvious at the normal border. Both PAR-1 and PAR-2 were expressed in the microvessel endothelial cells in tumors. Trypsin mRNA was expressed in 7 of the 16 cancer cell-bearing tissue specimens in contrast to 1 of the 14 normal alveolar walls. Immunohistochemically, trypsin was positive in the neoplastic cells from 10 patients and in lung adenocarcinoma cell lines (A549, HLC-1, LC-2, and PC-14). An in vitro assay showed a significant increase in idoxuridine (IdU) or bromodeoxyuridine uptake in human pulmonary artery endothelial cells and human umbilical cord vein endothelial cells after treatments with alpha-thrombin or activating peptides; SFLLRN for PAR-1 and SLIGKV for PAR-2, respectively. |
| T4 | 1663-1937 | CONCLUSIONS | denotes | Thus, proliferation of alveolar capillary endothelial cells is initialized in part by PAR activation with serum thrombin and neoplastic cell-released trypsin. These results suggest a synergistic effect of PAR with vascular endothelial growth factor in alveolar angiogenesis. |