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Published Erratum
. 2024 Sep:107:105303.
doi: 10.1016/j.ebiom.2024.105303. Epub 2024 Aug 13.

Corrigendum to "Autocrine CTHRC1 activates hepatic stellate cells and promotes liver fibrosis by activating TGF-β signaling" [EBioMedicine 40 (2019) 43-55]

Affiliations
Published Erratum

Corrigendum to "Autocrine CTHRC1 activates hepatic stellate cells and promotes liver fibrosis by activating TGF-β signaling" [EBioMedicine 40 (2019) 43-55]

Jun Li et al. EBioMedicine. 2024 Sep.
No abstract available

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Figures

Fig. 4
Fig. 4
CTHRC1 activates both TGF-β and Wnt signaling, while the promotive effect of CTHRC1 on HSC activation is mainly dependent on TGF-β signaling. A. The expression of α-SMA in primary HSCs after 7 days isolated from WT and CTHRC1−/− mice. B. The expression of α-SMA in primary rat HSCs after 4 days, which were treated with vehicle, 20 nM rCTHRC1 protein alone, and 20 nM rCTHRC1 protein plus CTHRC1 mAb or IgG. C. Western blotting analysis of phosphorylation of Smad2, Smad3, JNK, total Smad4 and expression of Wnt5a in five liver tissues of WT or CTHRC1−/− mice intraperitoneally injected with CCl4. GAPDH was the loading control. The densitometry of p-Smad2/Smad2 was shown below. D. Phosphorylation of Smad2, Smad3, JNK, total Smad4 and expression of Wnt5a in primary rat HSCs, which were treated with vehicle, 20 nM rCTHRC1 protein, and 20 nM rCTHRC1 protein plus CTHRC1 mAb or IgG for 1, 3, 5 days, individually. GAPDH was the loading control. The densitometry of p-Smad2/Smad2 was shown below. E and F. Representative immunofluorescence images of α-SMA (green in E, red in F) in primary rat HSCs after 4 days, which were treated with vehicle, 20 nM rCTHRC1 protein, and 20 nM rCTHRC1 protein plus neutralizing antibodies or inhibitor as follows: TGFBR2 neutralizing antibody or TGF-β receptor inhibitor (E), Wnt5a or Wnt3a neutralizing antibody (F). Nuclei are stained with DAPI (blue). Scale bars, 50 μm. G. The expression of α-SMA in primary rat HSCs after 4 days, which were treated with vehicle, 20 nM rCTHRC1 protein, and 20 nM rCTHRC1 protein plus TGFBR2 neutralizing antibody or TGF-β receptor inhibitor. GAPDH was the loading control.
Fig. 5
Fig. 5
CTHRC1 monoclonal antibody attenuates promotive effects of CTHRC1 on liver fibrosis. A and B. Sirius red and Masson's trichrome staining in the livers of WT, WT C57 mice treated with CCl4 (A) or TAA (B) and intraperitoneally injected with monoclonal antibody (mAb) of CTHRC1 (n = 10) or IgG (n = 10). Each mouse was intraperitoneally injected with CTHRC1 mAb at a dose of 5 μg/g body weight. Scale bars, 100 μm. Quantification of sirius red and Masson's trichrome staining was shown right. C. The serum levels of ALT and AST in WT C57 mice treated with CCl4 or TAA and intraperitoneally injected with mAb of CTHRC1 (n = 10) or IgG (n = 10). D. The hepatic levels of Acta2, Col1a1, Timp1 and Mmp9 mRNA in WT C57 mice treated with CCl4 or TAA and intraperitoneally injected with CTHRC1 mAb (n = 10) or IgG (n = 10) were determined by qPCR. E. Immunohistochemical staining of α-SMA and desmin in CCl4 (E, upper photos) and TAA (E, lower photos) induced liver fibrosis tissues of WT mice treated with CTHRC1 blocking antibody or IgG control, using serial sections. Scale bars, 100 μm. Quantification of immunostaining was shown below. F. Western blotting analysis of phosphorylation of Smad2, Smad3 and total Smad4 in five liver tissues of WT mice treated with CTHRC1 mAb or IgG. GAPDH was detected as the loading control. The densitometry of p-Smad2/Smad2 was shown below. ∗∗P < 0.01.

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