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. 2021 Jun 9;12(4):1297–1310. doi: 10.1016/j.jcmgh.2021.06.003

Figure 8.

Figure 8

Hepatocyte YAP depletion hinders fibrosis progression in NAFLD. (A) Representative microscopic photographs of liver sections stained with picrosirius red, Oil red O, and hematoxylin and eosin in liver tissue from Albumin-Cre;YapWT/WT (YAP-WT) or Albumin-Cre;Yapflox/flox (YAP-KO) mice fed standard chow or CDAHFD for 14 weeks (original magnification ×10). Percent of picrosirius red–stained liver tissue is graphed as mean ± SD (n = 3 mice per group; ∗∗P < .01, ∗∗∗P < .001). (B) Immunoblot and reverse-transcription polymerase chain reaction analyses of extracellular matrix-related (Acta2, Col1a1), fibrogenic (Ctgf, Pdgf, Vegfb), proinflammatory (Cyr61, Il6), and YAP-dependent (Ctgf, Cyr61, Il6) gene expression in liver samples from mice in (A). Mean ± SD are graphed (n = 3 mice per group, ∗P < .05, ∗∗P < .01). (C) Immunoblot and reverse-transcription polymerase chain reaction analyses of YAP, ANKRD1, CYR61, CTGF, JUB, and TGFB1 expression in Huh7 cells stably transduced with NT or YAP shRNA (shYAP-2 or 5) lentiviral particles. Mean ± SD are graphed (n = 3 biological replicates; ∗P < .05, ∗∗P < .01). (D) mRNA expression of COL1A1, CO3A1, ACTA2, and TIMP1 in spheroids consisting of Huh7 cells stably transduced with shYAP-5 (shY5) and pHSCs. Mean ± SD are graphed (n = 3 biological replicates; ∗P < .05, ∗∗P < .01).