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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. 5 — BetA increases the TGF-β-induced nuclear translocation of Smad2 in Mv1Lu cells. After 1 h of incubation of cells with 5 μg/mL BetA followed by 30 min of treatment with 20 pM TGF-β, the cells were fixed, subjected to immunofluorescence staining with primary antibodies against Smad2 as well as secondary antibodies linked to FITC, and mounted with a DAPI-containing medium. FITC fluorescence represents P-Smad2 staining (A, panels a-e), whereas the nuclei were subjected to DAPI staining (A, panels f-j). The nuclear/cytoplasm ratio of the Smad2 level was determined among 100 cells in 10 different fields, and were quantified using Image J (NIH, Bethesda, MD) (B). Values are expressed as the mean ± SD (n = 3). **The group of BetA/ TGF-β co-treatment significantly higher than that in cells treated with TGF-β only (P < 0.01)