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. 2021 Feb 16;11:3857. doi: 10.1038/s41598-021-83516-2

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© The Author(s) 2021

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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Regulation of CTGF through YAP in LX2 cells treated with Si-RNA or YAP inhibitor Verteporfin under hypoxia for 3 h and reoxygenation for 1 h. LX2 cells treated with vehicle of Si-RNA or Verteporfin were regarded as control. (A) Changes of YAP and CTGF mRNAs in LX2 cells after YAP-siRNA treatment under hypoxia/reoxygenation determined by RT-qPCR (*P < 0.05 between siRNA and control). (B) Changes of CTGF, YAP, and p-YAP protein levels after YAP-siRNA treatment in LX2 cells determined by WB (*P < 0.05 between siRNA and control). (C) Immunofluorescence staining of CTGF (green) and YAP (red) in LX2 cells under hypoxia/reoxygenation; DAPI (blue) was used for nuclear staining (scale bar = 20 μm, ×200 magnification) and semi-quantitation of nuclear YAP (*P < 0.05). (D) Changes of CTGF, YAP, and p-YAP expression in LX2 cells after treatment of the YAP inhibitor Verteporfin under hypoxia/reoxygenation (*P < 0.05). (E) Schematic of the proposed mechanism of CTGF regulation in the non-steatotic liver after brain death.