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Cell-based Angiopoietin-1 Gene Therapy for Acute Lung Injury

McCarter, Sarah D., Mei, Shirley H. J., Lai, Patrick F. H., Zhang, Qiu Wang, Parker, Colleen H., Suen, Renée S., Hood, Roberta D., Zhao, Yidan D., Deng, Yupu, Han, Robin N. N., Dumont, Daniel J., Stewart, Duncan J.·2007·American Journal of Respiratory and Critical Care Medicine

DOI 10.1164/rccm.200609-1370oc

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Abstract

Rationale: The acute respiratory distress syndrome is a significant cause of morbidity and mortality in critically ill patients. Angiopoietin-1 (Ang-1), a ligand for the endothelial Tie2 receptor, is an endothelial survival and vascular stabilization factor that reduces endothelial permeability and inhibits leukocyte–endothelium interactions. Objectives: We hypothesized that Ang-1 counteracts vascular inflammation and pulmonary vascular leak in experimental acute lung injury. Methods: We used cell-based gene therapy in a rat model of ALI. Transgenic mice overexpressing Ang-1 or deficient in the Tie2 receptor were also studied to better elucidate the mechanisms of protection. Measurements and Main Results: The present report provides data that support a strong protective role for the Ang-1/Tie2 system in two experimental models of LPS-induced acute lung injury. In a rat model, cell-based Ang-1 gene transfer improved morphological, biochemical, and molecular indices of lung injury and inflammation. These findings were confirmed in a gain-of-function conditional, targeted transgenic mouse model, in which Ang-1 reduced endothelial cell activation and the expression of adhesion molecules, associated with a marked improvement in airspace inflammation and intraalveolar septal thickening. Moreover, heterozygous Tie2-deficient mice demonstrated enhanced evidence of lung injury and increased early mortality. Conclusions: These results support a critical role for the Ang-1/Tie2 axis in modulating the pulmonary vascular response to lung injury and suggest that Ang-1 therapy may represent a potential new strategy for the treatment and/or prevention of acute respiratory distress syndrome in critically ill patients.

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Authors: McCarter, S. D., Mei, S. H. J., Lai, P. F. H., Zhang, Q. W., Parker, C. H., Suen, R. S., Hood, R. D., Zhao, Y. D., Deng, Y., Han, R. N. N., Dumont, D. J., & Stewart, D. J.
Affiliations: St. Michael's Hospital (CA)
Sunnybrook Research Institute (CA)
ORCID: Mei, Shirley H. J.
Lai, Patrick F. H.
Parker, Colleen H.
Zhao, Yidan D.
Han, Robin N. N.
Dumont, Daniel J.
Stewart, Duncan J.
Venue: American Journal of Respiratory and Critical Care Medicine
Publisher: Oxford University Press (OUP)
Published: 2007-05
Volume: 175
Issue: 10
Pages: 1014-1026
ISSN: 1073-449X (ISSN-L)
1535-4970
DOI: 10.1164/rccm.200609-1370oc
OpenAlex: W2038968218
Cited by: 154
References: 54
Citations by year: 2026: 1 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 9 · 2020: 8 · 2019: 4 · 2018: 11 · 2017: 4 · 2016: 9 · 2015: 9 · 2014: 4 · 2013: 11 · 2012: 11
FWCI: 12.27
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: American Journal of Respiratory and Critical Care Medicine (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Keywords: angiopoietin-1, Tie2 receptor, acute lung injury, acute respiratory distress syndrome, cell-based gene therapy, endothelial inflammation, leukocyte-endothelial adhesion, lipopolysaccharide-induced lung injury, endothelial activation, adhesion molecules, transgenic mouse model
MeSH terms: Animals, Cell Adhesion, Female, Fibroblasts, Lipopolysaccharides, Male, Mice, Transgenic, Rats, Inbred F344, Respiratory Distress Syndrome, Genetic Therapy, Cell Adhesion Molecules, Gene Expression, Cytokines, Angiopoietin-1, Receptor, TIE-2, Mice, Rats

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Cell-based Angiopoietin-1 Gene Therapy for Acute Lung Injury

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