期刊
FEBS LETTERS
卷 579, 期 18, 页码 4031-4037出版社
WILEY
DOI: 10.1016/j.febslet.2005.06.018
关键词
pulmonary endothelium; TGF beta 1; ALK1 and 5; Smad4; permeability; actin
资金
- NHLBI NIH HHS [HL080675, HL58064, HL67307, HL68062] Funding Source: Medline
The ability of inflammatory cytokine TGF-beta 1 to alter endothelial cell phenotype suggests its role in the regulation of vascular endothelial cell permeability. We demonstrate that depletion of TGF-beta 1 receptor ALK5 and regulatory protein Smad4, but not ALK1 receptor attenuates TGF-beta 1-induced permeability increase and significantly inhibits TGF-beta 1-induced EC contraction manifested by actin stress fiber formation and increased MLC and MYPT1 phosphorylation. Consistent with these results, EC treatment with SB 431542, an inhibitor of ALK5 but not ALK1 receptor, significantly attenuates TGFP1-induced permeability. Thus, our data demonstrate for the first time direct link between TGF-beta 1-mediated activation of ALK5/Smad and EC barrier dysfunction. (c) 2005 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
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