Compounds > 12-hydroxy-5-8-10-14-eicosatetraenoic-acid

12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Graft-Occlusion--Vascular

12-hydroxy-5-8-10-14-eicosatetraenoic-acid has been researched along with Graft-Occlusion--Vascular* in 1 studies

Other Studies

1 other study(ies) available for 12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Graft-Occlusion--Vascular

Article	Year
Aspirin enhances platelet-derived growth factor-induced vascular smooth muscle cell proliferation. Journal of vascular surgery, 1997, Volume: 25, Issue:4 Aspirin is frequently used after vascular reconstruction to pharmacologically prevent graft occlusion and to suppress the development of myointimal hyperplasia in vascular surgery, but its efficacy is controversial. The purpose of this study was to examine the direct effects of aspirin on platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell (SMC) proliferation.. Human aortic SMCs were grown to confluence in 96 well plates. 3 x 10(-5) mol/L aspirin was added 24 hours previously and PDGF 10 ng/ml at the beginning of each experiment. Cell proliferation at 48 hours was determined using tritiated thymidine uptake. Supernatant 12-L-hydroxy 5,8,10,14-eicosatetraenoic acid (12-HETE) and prostaglandin E2 (PGE2) were measured by competitive enzyme immunoassay.. Aspirin did not change vascular SMC proliferation rates relative to controls (4665 +/- 181 counts per minute [CPM] vs 4749 +/- 155 CPM). However, aspirin pretreatment of PDGF-stimulated vascular SMCs increased proliferation (9408 +/- 237 CPM vs 7283 +/- 283 CPM; p < 0.001). 5,8,10,14-eicosatriynoic acid, a 12-lipoxygenase inhibitor, decreased basal (2037 +/- 181 CPM vs 2306 +/- 158 CPM; p < 0.05) and PDGF-stimulated vascular SMC proliferation (4909 +/- 1089 CPM vs 4310 +/- 1022 CPM; p < 0.001). Aspirin increased supernatant 12-HETE levels and decreased PGE2 levels in both basal and PDGF-stimulated cell cultures.. Aspirin enhances PDGF-stimulated vascular SMC proliferation. The effects of aspirin on vascular SMC proliferation may be mediated by changes in vascular SMC arachidonic acid metabolism. Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Aorta; Arachidonate 12-Lipoxygenase; Arachidonic Acids; Aspirin; Cell Division; Cells, Cultured; Cyclooxygenase Inhibitors; Dinoprostone; Drug Synergism; Graft Occlusion, Vascular; Humans; Hyperplasia; Multivariate Analysis; Muscle, Smooth, Vascular; Platelet Aggregation Inhibitors; Platelet-Derived Growth Factor; Regression Analysis; Thymidine; Tritium; Tunica Intima; Vascular Surgical Procedures	1997

Article

Year

Aspirin enhances platelet-derived growth factor-induced vascular smooth muscle cell proliferation.

Journal of vascular surgery, 1997, Volume: 25, Issue:4

Aspirin is frequently used after vascular reconstruction to pharmacologically prevent graft occlusion and to suppress the development of myointimal hyperplasia in vascular surgery, but its efficacy is controversial. The purpose of this study was to examine the direct effects of aspirin on platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell (SMC) proliferation.. Human aortic SMCs were grown to confluence in 96 well plates. 3 x 10(-5) mol/L aspirin was added 24 hours previously and PDGF 10 ng/ml at the beginning of each experiment. Cell proliferation at 48 hours was determined using tritiated thymidine uptake. Supernatant 12-L-hydroxy 5,8,10,14-eicosatetraenoic acid (12-HETE) and prostaglandin E2 (PGE2) were measured by competitive enzyme immunoassay.. Aspirin did not change vascular SMC proliferation rates relative to controls (4665 +/- 181 counts per minute [CPM] vs 4749 +/- 155 CPM). However, aspirin pretreatment of PDGF-stimulated vascular SMCs increased proliferation (9408 +/- 237 CPM vs 7283 +/- 283 CPM; p < 0.001). 5,8,10,14-eicosatriynoic acid, a 12-lipoxygenase inhibitor, decreased basal (2037 +/- 181 CPM vs 2306 +/- 158 CPM; p < 0.05) and PDGF-stimulated vascular SMC proliferation (4909 +/- 1089 CPM vs 4310 +/- 1022 CPM; p < 0.001). Aspirin increased supernatant 12-HETE levels and decreased PGE2 levels in both basal and PDGF-stimulated cell cultures.. Aspirin enhances PDGF-stimulated vascular SMC proliferation. The effects of aspirin on vascular SMC proliferation may be mediated by changes in vascular SMC arachidonic acid metabolism.

Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Aorta; Arachidonate 12-Lipoxygenase; Arachidonic Acids; Aspirin; Cell Division; Cells, Cultured; Cyclooxygenase Inhibitors; Dinoprostone; Drug Synergism; Graft Occlusion, Vascular; Humans; Hyperplasia; Multivariate Analysis; Muscle, Smooth, Vascular; Platelet Aggregation Inhibitors; Platelet-Derived Growth Factor; Regression Analysis; Thymidine; Tritium; Tunica Intima; Vascular Surgical Procedures

1997