The Library
Type XVIII collagen degradation products in acute lung injury
Tools
Tools
Tools
Perkins, Gavin D., Nathani, Nazim, Richter, Alex G., Park, Daniel, Shyamsundar, Murali, Heljasvaara, Ritva, Pihlajaniemi, Taina, Manji, Mav, Tunnicliffe, W., McAuley, Danny, Smith, F. Gao (Fang Gao) and Thickett, David R. (2009) Type XVIII collagen degradation products in acute lung injury. Critical Care, 13 (2). R52. doi:10.1186/cc7779 ISSN 1466-609X.
Research output not available from this repository.
Request-a-Copy directly from author or use local Library Get it For Me service.
Official URL: http://dx.doi.org/10.1186/cc7779
Abstract
Introduction:
In acute lung injury, repair of the damaged alveolar-capillary barrier is an essential part of recovery. Endostatin is a 20 to 28 kDa proteolytic fragment of the basement membrane collagen XVIII, which has been shown to inhibit angiogenesis via action on endothelial cells. We hypothesised that endostatin may have a role in inhibiting lung repair in patients with lung injury. The aims of the study were to determine if endostatin is elevated in the plasma/bronchoalveolar lavage fluid of patients with acute lung injury and ascertain whether the levels reflect the severity of injury and alveolar inflammation, and to assess if endostatin changes occur early after the injurious lung stimuli of one lung ventilation and lipopolysaccharide (LPS) challenge.
Methods:
Endostatin was measured by ELISA and western blotting.
Results:
Endostatin is elevated within the plasma and bronchoalveolar lavage fluid of patients with acute lung injury. Lavage endostatin reflected the degree of alveolar neutrophilia and the extent of the loss of protein selectivity of the alveolar-capillary barrier. Plasma levels of endostatin correlated with the severity of physiological derangement. Western blotting confirmed elevated type XVIII collagen precursor levels in the plasma and lavage and multiple endostatin-like fragments in the lavage of patients. One lung ventilation and LPS challenge rapidly induce increases in lung endostatin levels.
Conclusions:
Endostatin may adversely affect both alveolar barrier endothelial and epithelial cells, so its presence within both the circulation and the lung may have a pathophysiological role in acute lung injury that warrants further evaluation.
| Item Type: | Journal Article | ||||
|---|---|---|---|---|---|
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Clinical Trials Unit Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Health Sciences Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
||||
| Journal or Publication Title: | Critical Care | ||||
| Publisher: | BioMed Central Ltd. | ||||
| ISSN: | 1466-609X | ||||
| Official Date: | 2009 | ||||
| Dates: |
|
||||
| Volume: | 13 | ||||
| Number: | 2 | ||||
| Article Number: | R52 | ||||
| DOI: | 10.1186/cc7779 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Open Access (Creative Commons) |
Request changes or add full text files to a record
Repository staff actions (login required)
 |
View Item |
