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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Endothelin-1 induces expression of matrix- associated genes in lung fibroblasts through MEK/ ERK.

The endothelins are a family of endothelium-derived peptides that possess a variety of biological activities, including potent vasoconstriction. Endothelin-1 (ET-1) is up-regulated during tissue repair and pulmonary fibrosis. Here, we use genome-wide expression array analysis to show that the addition of ET-1 (100 nm, 4 h) to normal lung fibroblasts directly induces expression of matrix and matrix-associated genes, including the profibrotic protein CCN2 (connective tissue growth factor, or CTGF). ET-1 induces the MEK/ ERK MAP kinase pathway in fibroblasts. Blockade of the MEK/ ERK kinase pathway with U0126 abrogates the ability of ET-1 to induce expression of matrix and matrix- associated mRNAs and the CCN2 protein. The CCN2 promoter possesses an ET-1 response element, which maps to the previously identified basal control element-1 (BCE-1) site. Our results suggest that ET-1 induces a program of matrix synthesis in lung fibroblasts and that ET-1 may play a key role in connective tissue deposition during wound repair and in pulmonary fibrosis.[1]

References

  1. Endothelin-1 induces expression of matrix-associated genes in lung fibroblasts through MEK/ERK. Xu, S.W., Howat, S.L., Renzoni, E.A., Holmes, A., Pearson, J.D., Dashwood, M.R., Bou-Gharios, G., Denton, C.P., du Bois, R.M., Black, C.M., Leask, A., Abraham, D.J. J. Biol. Chem. (2004) [Pubmed]
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