The study of endothelial cell signal transduction during neutrophil transmigration
Project/Area Number |
12671295
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Thoracic surgery
|
Research Institution | Akita University |
Principal Investigator |
KAMATA Skuichi Akita University, School of Medicine, Research Associate, 医学部, 助手 (00224650)
|
Co-Investigator(Kenkyū-buntansha) |
MINAMIYA Yoshihiro Akita University, School of Medicine, Associate Professor, 医学部, 助教授 (30239321)
OGAWA Jun-ichi Akita University, School of Medicine, Professor, 医学部, 教授 (20112774)
|
Project Period (FY) |
2000 – 2001
|
Project Status |
Completed (Fiscal Year 2001)
|
Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
Keywords | neutrophils / endothelial cell / transmigration / Rho / Rho kinase / F-actin / Myosin II / MLC |
Research Abstract |
The transendothelial migration of neutrophils is a critical step in acute inflammation, which we previously showed to be regulated by endothelial myosin light chain kinase. Recent studies suggest that Rho and Rho kinase are also key mediators of myosin light chain (MLC) phosphorylation, but their roles in neutrophil migration has not been investigated. In the present study, a transwell chamber migration assay system incorporating endothelial monolayer was used to examined the numbers of migrating neutrophils, endothelial F-actin and myosin II rearrangement and endothelial MLC phosphorylation at selected times during the neutrophil migration, in vitro. The results showed that pretreating endothelial cells with C3 (Rho inhibitor) or Y-27632 (Rho kinase inhibitor) significantly diminished neutrophil migration, actin polymerization, myosin II filament formation and MLC phosphorylation normally associated with the migration. These data suggest that endothelial Rho and Rho kinase regulate transendothelial neutrophil migration by modulating the cytoskeletal events that mediate such migration.
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Report
(3 results)
Research Products
(3 results)