Premium
Angiopoietin‐1 reverses protein permeability in an injury model of cultured human alveolar epithelial type II cells
Author(s) -
Neyrinck Arne Pieter,
Lee JaeWoo,
Fang Xiaohui,
Gupta Naveen,
Matthay Michael A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.932.6
Subject(s) - vascular permeability , permeability (electromagnetism) , recombinant dna , pharmacology , chemistry , in vitro , pulmonary edema , lung , biology , medicine , endocrinology , biochemistry , membrane , gene
OBJECTIVE: We recently reported that acute lung injury (ALI) pulmonary edema and cytomix (IL1β, TNFα and IFNγ) increase epithelial protein permeability (JBC, 2007). Angiopoietin‐1 (Ang‐1) maintains vascular integrity and reduces endothelial activation in a model of ALI (AJRCCM 2007). In this study, we hypothesized that Ang‐1 could reverse increased protein permeability in cultured human alveolar epithelial type II cells (ATII) exposed to cytomix. METHODS: Isolated human ATII cells were cultured in an air‐liquid interface and protein permeability was measured. Cells were exposed to control medium, cytomix (50 ng/ml) and cytomix with recombinant human Ang‐1 (10,000 pg/ml). RESULTS: 1) Cytomix increased protein permeability in cultured ATII cells. 2) Recombinant human Ang‐1 decreased ATII protein permeability significantly after exposure to cytomix (Figure 1). CONCLUSIONS: Ang‐1 can reverse protein permeability across ATII cells exposed to cytomix. These results are the first results to show a potential role for Ang‐1 in regulation of alveolar epithelial permeability. The data support a further role of Ang‐1 in the treatment of ALI. Supported by NIH HL51856 and HL51854