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. 2020 Dec 23;10:22373. doi: 10.1038/s41598-020-79450-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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S. mansoni egg-induced expression of proliferation markers. (a,b) Increased enterocyte proliferation, denoted by Cyclin D1-immunostaining adjacent [red arrowheads in (b)] to the eggs (*) was distinct from physiological proliferation of enterocytes in basal crypts [black arrowheads in (a)]. Representative cross sections of colon mucosa from hamsters are shown.(a) single sex-infected control, (b) bisex-infected. Magnification 200×, bar 2200 µm and 1000×, bar 20 µm. (c) Western blot analysis and subsequent semi-quantitative assessment of optical density suggested an enhanced expression of Cyclin D1 and Mcm2 in the colon of S. mansoni bisex-infected hamsters in comparison to single sex-infected controls. Representative blots are shown, control n = 4, bisex infection n = 11. Differences were analyzed statistically between control and bisex-infected for Cyclin D1/Gapdh and Mcm2/Gapdh. *p ≤ 0.05. (d) The expression of Cyclin D1 was induced by SEA and could be inhibited by additional treatment with the JNK-inhibitor SP600125 (upper blots) and the MEK-inhibitor U0126 (lower blots) in SW620 cells. The cells were pretreated with inhibitors for 30 min and subsequently during stimulation for 4 h. (e) The expression of Cyclin D1 was also induced by nIPSE. (f) SEA-stimulated Cyclin D1 expression was reduced by tankyrase inhibition, using XAV939, in SW620 cells. IPSE-induced Cyclin D1 expression, however, was not reduced by tankyrase inhibition. The cells were pretreated with XAV939 for 15 h and subsequently during stimulation for 4 h. The experiment and assay was reproduced at least two times. Representative western blots are shown.