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. 2020 Jan 28;69(9):1677–1690. doi: 10.1136/gutjnl-2019-319091

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Impact of AON-mediated TgfB2 silencing on collagen expression and deposition as well as αSMA expression in MDR2-KO mice. (A) Hydroxyproline (HYP) content in the liver of AON-treated MDR2-KO mice was significantly downregulated compared with untreated and control oligo-treated animals. (B) Sirius red staining (pSR) revealed significant downregulation (~56%) of collagen deposition in the tissue of AON-treated compared with untreated MDR2-KO mice. Scale bars indicate 500 µm. (C) Immunohistochemical staining demonstrated a decrease of αSMA expression in AON-treated animals of 35% compared with untreated animals and 43% compared with animals treated with control oligos. Scale bars indicate 200 µm. (D) Reduction was verified by immunoblot analysis. *p≤0.05, **p≤0.01, ***p≤0.001. AON, antisense oligonucleotides; MDR2-KO, multidrug resistance gene 2 knockout; SMA, smooth muscle actin; TGFB, transforming growth factor beta.