Mechanism for the Increased Permeability in Endothelial Monolayers Induced by Elastase
The aim of this study was to investigate the mechanism for the increase in endothelial permeability induced by human neutrophil elastase (HNE). Pretreatment of bovine pulmonary artery endothelial cells (BPAEC) with HNE(0-30 μg/ml) for 1 h produced a concentration dependent increase in 125I-albumin c...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935194000025 |
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| Summary: | The aim of this study was to investigate the mechanism for the
increase in endothelial permeability induced by human neutrophil
elastase (HNE). Pretreatment of bovine pulmonary artery endothelial
cells (BPAEC) with HNE(0-30 μg/ml) for 1 h produced a concentration
dependent increase in 125I-albumin clearance. The effect was
reversible and was not due to cytolysis. Pretreatment of BPAEC with
sodium tungstate, which depletes xanthine oxidase, or with
oxypurinol, did not prevent HNE induced increased permeability.
Heparin, which neutralizes the cationic charge of HNE, also had no
protective effect. Pretreatment with heat inactivated HNE, which
still had positive charge sites, did not result in increased
endothelial permeability. Also, ONO-5046, a novel specific inhibitor
of HNE, did prevent increased permeability. These results suggest
that elastase increases endothelial permeability mainly through its
proteolytic effects. |
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| ISSN: | 0962-9351 1466-1861 |