Copyright
©The Author(s) 2016.
World J Gastroenterol. Mar 7, 2016; 22(9): 2779-2788
Published online Mar 7, 2016. doi: 10.3748/wjg.v22.i9.2779
Published online Mar 7, 2016. doi: 10.3748/wjg.v22.i9.2779
Figure 2 Chronic CCl4 injury suppresses Gadd45a expression and activates TGF-β/Smad signaling.
A: Relative mRNA expression levels of Gadd45a, Gadd45b, and Gadd45g in the livers of mice treated with CCl4 for 1, 2, and 4 wk; the saline-treated group served as the control group; B: Relative protein expression levels of Gadd45a, Gadd45b, and Gadd45g in the livers of mice treated with CCl4 for 1, 2, and 4 wk; C: Immunofluorescence staining of Gadd45a, Gadd45b, and Gadd45g (in green) in HSCs treated with CCl4 for 4 wk (nuclei are stained blue with DAPI; scale bars = 10 μm); D: Expression levels of p-Smad2, p-Smad3, Smad2, Smad3, and Smad4 were analyzed in HSCs treated with CCl4 for 1, 2, and 4 wk. HSC: Hepatic stellate cells; TGF: Transforming growth factor.
- Citation: Hong L, Sun QF, Xu TY, Wu YH, Zhang H, Fu RQ, Cai FJ, Zhou QQ, Zhou K, Du QW, Zhang D, Xu S, Ding JG. New role and molecular mechanism of Gadd45a in hepatic fibrosis. World J Gastroenterol 2016; 22(9): 2779-2788
- URL: https://www.wjgnet.com/1007-9327/full/v22/i9/2779.htm
- DOI: https://dx.doi.org/10.3748/wjg.v22.i9.2779