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. 2016 Feb 27;23:30. doi: 10.1186/s12929-016-0229-4

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© Chen et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — BetA enhances the TGF-β response downstream of ALK-5 in Mv1Lu cells. Cells stably expressing the PAI-1 luciferase promoter were transiently transfected with caALK-5 or pcDNA3.1 (as a control). These transfected cells exhibited a potent luciferase activity in the absence of exogenously added TGF-β. BetA appeared to enhance caALK-5-stimulated PAI-1 (a and b), fibronectin (c), and collagen (d) promoter luciferase expression in a concentration-dependent manner. Cholesterol treatment suppressed the BetA-enhanced luciferase activity. The data bar represents the mean ± SD from four different analyses. * and **Significantly higher than that in cells treated without BetA (a) or lower than that in cells treated without cholesterol (b, c, and d) (*: P < 0.05, **: P < 0.01)