Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Reactive oxidant species (ROS) release from fMLP-stimulated neutrophils increases microvessel permeability via nitric oxide (NO)-cGMP-dependent pathway.

Authors
Zhu-L; Castranova-V; He-P
Source
FASEB J 2004 Mar; 18(4)(Suppl):A245
NIOSHTIC No.
20031567
Abstract
Our previous study demonstrated that ROS release from fMLP-stimulated neutrophils increases microvessel permeability independently from leukocyte adhesion and migration. We hypothesized that the activation of NO-cGMP-dependent signaling pathway in endothelial cells is the mechanism and that enhancing endothelial cAMP levels may overcome its activation and prevent the ROS-induced permeability increase. ROS production from fMLP-stimulated rat neutrophils was quantified by measuring chemiluminescence. Changes in permeability after microvessels were perfused with fMLP-stimulated neutrophil suspensions with and without the inhibition of endothelial eNOS or guanylate cyclase were measured as hydraulic conductivity in individually perfused rat mesenteric venular microvessels. The application of guanylate cyclase inhibitor, LY-83583, did not reduce the ROS release from fMLP stimulated neutrophils, but abolished ROS-induced permeability increase. Similar results were obtained with inhibition of endothelial eNOS activity by internalization of caveolin-1 scaffolding domain in individually perfused microvessels. Enhancing endothelial cAMP levels by the application of an beta-adrenergic agonist, isoproteronol, prevented the permeability increase. These results indicate that ROS-induced increases in microvessel permeability involve the activation of a NO-cGMP-dependent signaling pathway, which can be counteracted by enhancing endothelial cAMP levels.
Keywords
Cell-function; Cell-metabolism; Cell-transformation; Cell-wall-permeability; Chemical-hypersensitivity; Chemical-properties; Gas-adsorption
CODEN
FAJOEC
Publication Date
20040323
Document Type
Abstract
Fiscal Year
2004
NTIS Accession No.
NTIS Price
Issue of Publication
4
ISSN
0892-6638
NIOSH Division
HELD
Source Name
The FASEB Journal. Experimental Biology 2004, Washington, DC, April 17-21, 2004
State
WV; SC
TOP