Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 107, Issue 12, Pages 1537-1544Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI11963
Keywords
-
Categories
Funding
- NHLBI NIH HHS [HL-53949, T32 HL-07185, R01 HL051854, R01 HL053949, HL-33259, HL-51854, T32 HL007185, HL-47412, R37 HL053949] Funding Source: Medline
Ask authors/readers for more resources
We have shown that the integrin alphav betaG activates latent TGF-beta in the lungs and skin. We show here that mice lacking this integrin are completely protected from pulmonary edema in a model of bleomycin-induced acute lung injury (ALI). Pharmacologic inhibition of TGF-beta also protected wild-type mice from pulmonary edema induced by bleomycin or Escherichia coli endotoxin. TGF-beta directly increased alveolar epithelial permeability in vitro by a mechanism that involved depletion of intracellular glutathione. These data suggest that integrin-mediated local activation of TGF-beta is critical to the development of pulmonary edema in ALI and that blocking TGF-beta or its activation could be effective treatments for this currently untreatable disorder.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available