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. 2008 Sep 16;99(9):1375–1379. doi: 10.1038/sj.bjc.6604662

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Copyright © 2008 Cancer Research UK

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Endothelial-to-mesenchymal transition in cancer and cardiac fibrosis. (A) The Tie2-Cre;ROSA-STOP-lacZ reporter mouse is an important strain for tracking cells of endothelial origin during EndMT. In this mouse, Cre expression is driven by the Tie2 promoter, which is known to be active in endothelial cells. The Cre recombinase acts by permanently excising genomic DNA regions that are flanked by loxP sites (floxed). In this case, Tie2-driven Cre activity removes a floxed stop cassette, thereby allowing lacZ expression to be driven by the constitutive ROSA26R promoter (ROSA) without the need for continued Tie2 activity. (B) During cardiac fibrosis, TGF-β signalling promotes EndMT through Smad3 transcriptional activity. In endothelial cells, TGF-β is known to activate Alk5, which then activates Smad3. However, the role of Alk5 has not been explicitly demonstrated during EndMT in cardiac fibrosis. EndMT was also shown to be inhibited by rhBMP-7 (dashed lines). BMP-7 is known to act through a different set of Smads, namely Smad1, -5, and -8. However, the precise mechanisms whereby BMP-7 inhibits EndMT are not yet known.