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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. 2 — BetA enhances the transcriptional response stimulated by TGF-β in Mv1Lu cells. Cells stably expressing the PAI-1 luciferase reporter plasmid exhibited a 6-fold increase of the luciferase activity after stimulation with 100 pM TGF-β and the TGF-β-stimulated luciferase activity was enhanced by BetA in a concentration-dependent manner (a) and (b). However, the BetA-enhanced TGF-β-stimulated PAI-1 luciferase activity was diminished in the presence of cholesterol (b). Cells transiently transfected with the fibronectin (c) and collagen (d) luciferase reporter plasmids were treated with 100 pM TGF-β and increasing concentrations of BetA and/or cholesterol. BetA also enhanced the TGF-β-stimulated luciferase activity driven by the promoters of fibronectin (c) and collagen (d). The presence of cholesterol inhibited these BetA-enhanced luciferase activities (b, c, and d). The data bar represents the mean ± S.D. ** and * indicate the significant different between cells treated with or without BetA (a), or lower than that in cells treated without cholesterol in the same concentration of BetA group (b, c, and d) (*: P < 0.05, **: P < 0.01)