Fig. 2: Sestrin2 deficiency exacerbates cholestatic liver injury. | Experimental & Molecular Medicine

Fig. 2: Sestrin2 deficiency exacerbates cholestatic liver injury.

From: Sestrin2 protects against cholestatic liver injury by inhibiting endoplasmic reticulum stress and NLRP3 inflammasome-mediated pyroptosis

Fig. 2

A Immunofluorescence staining of cleaved caspase-3 (green, arrows) in HepG2 cells infected with lentiviruses expressing shRNAs targeting luciferase (sh-Luc) or Sestrin2 (sh-SESN2) and treated with 150 µM CDCA for 12 h (n = 4–5). Nuclei were counterstained with DAPI (blue). B, C qRT–PCR analysis of TGFB1 mRNA levels in HepG2 cells infected with sh-Luc or sh-SESN2 and treated with 200 µM CDCA or 750 µM CA for 12 h (n = 3). D–F Serum ALT, AST, and ALP levels in Sesn2+/+ Sham, Sesn2+/+ BDL, Sesn2−/− Sham, and Sesn2−/− BDL mice (n = 5-10 mice per group). G–J Sesn2+/+ and Sesn2−/− mice were subjected to sham or bile duct ligation (BDL) for 3 days (n = 5–12 mice per group). G Immunohistochemical analysis of cleaved caspase-3 in liver tissues from Sesn2+/+ Sham, Sesn2+/+ BDL, Sesn2−/− Sham, and Sesn2−/− BDL mice. The boxed areas are magnified in the bottom panels. H, I H&E-stained liver sections from Sesn2+/+ Sham, Sesn2+/+ BDL, Sesn2−/− Sham, and Sesn2−/− BDL mice. Areas of necrosis were quantified. H, J Sirius red staining showing collagen fiber deposition in liver tissues from Sesn2+/+ Sham, Sesn2+/+ BDL, Sesn2−/− Sham, and Sesn2−/− BDL mice. K qRT–PCR analysis of Tgfb1 mRNA levels in liver tissues from the indicated mice (n = 4–8 mice per group). Scale bars, 50 μm (a); 100 μm (G, H); 20 μm (G, insets). The data are representative of two (D–K) or three (A–C) independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant (two-way ANOVA, followed by Tukey’s (A–F, K) or Benjamini, Krieger, and Yekutieli’s (I, J) post hoc tests).

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