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Endothelium-derived microparticles induce endothelial dysfunction and acute lung injury
John C Densmore1, Paul R Signorino, Jingsong Ou
1Department of Surgery, Medical College of Wisconsin and Children's Hospital of Wisconsin, 9000 W. Wisconsin Avenue, Milwaukee, WI 53226, USA. jdensmore@mail.mcw.edu
Shock (Augusta, Ga.)
|October 19, 2006
Summary
Endothelium-derived microparticles (EMPs) impair blood vessel function and nitric oxide generation. These microparticles contribute to acute lung injury (ALI) by damaging endothelial cells and compromising the lung barrier.
Area of Science:
- Cardiovascular Biology
- Pulmonary Medicine
- Cellular Biology
Background:
- Acute lung injury (ALI) is a critical condition with high mortality.
- Endothelial dysfunction is linked to ALI, with elevated endothelium-derived microparticles (EMPs) implicated.
- EMPs may play a role in endothelial cell (EC) dysfunction and ALI development.
Purpose of the Study:
- To investigate the hypothesis that EMPs contribute to EC dysfunction and ALI.
- To determine the effects of EMPs on vasodilation, nitric oxide (*NO) production, and eNOS activation.
- To assess EMP-induced lung injury in rodent models.
Main Methods:
- Isolated mouse and human vessels were treated with EMPs to assess vasodilation.
- EC cultures were incubated with EMPs to measure *NO release and eNOS activation via Western analysis.
- Rats and mice were injected with EMPs, followed by analysis of lung permeability, myeloperoxidase activity, and histology.
Main Results:
- EMPs significantly attenuated endothelium-mediated vasodilation in ex vivo vessels.
- EMPs reduced stimulated *NO release and eNOS phosphorylation/hsp90 association in ECs.
- EMPs induced pulmonary edema, neutrophil recruitment, and compromised the endothelial-alveolar barrier in rats, consistent with ALI.
- EMPs increased pulmonary capillary permeability in mice, acting as both primary and secondary injury agents.
Conclusions:
- EMPs inhibit endothelium-mediated vasodilation and nitric oxide generation.
- EMPs can induce significant lung injury at pathophysiologically relevant concentrations.
- Understanding EMP mechanisms in ALI and endothelial dysfunction may reveal novel therapeutic targets.
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