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. 2017 May 18;8(5):e2792. doi: 10.1038/cddis.2017.10

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Knockdown of either TGFBR1 or TGFBR2 inhibited the TGF-β_/SMAD signaling pathway and reduced HSC activation. (a) Knockdown of TGFBR1 and/or TGFBR2 inhibited the mRNA and protein expression levels (b) of TGFBR1 and TGFBR2. β-actin was used as a loading control. Values represent the mean ±SD, ***P < 0.001 compared with control. (c) Knockdown of TGFBR1 and/or TGFBR2 inhibited the mRNA and protein expression levels (d) of α-SMA, Smad2, and Smad3. β-actin was used as a loading control. Values represent the mean ±SD, *P<0.05, **P<0.01, ***P<0.001 compared with control. (e) Knockdown of TGFBR1 and/or TGFBR2 inhibited the mRNA and protein levels (f) of MMP-2, MMP-9, Col-1, and Col-4. β-actin was used as a loading control. Values represent the mean±S.D., ***P<0.001 compared with control