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. 2020 Feb 24;21(4):1533. doi: 10.3390/ijms21041533

Figure 2.

Figure 2

Beclin1 heterozygosity leads to liver disorders in adult males. (A) (a–c) Representative pictures of 6-month-old male zebrafish. (d–f) The liver phenotypes in dissected males. (g–i) hematoxylin and eosin (H&E) histological staining of zebrafish livers and the beginning of bile ductus sequestration (arrowheads). (B) (a–c) Representative pictures of 12-month-old male zebrafish. beclin1+/− has enlarged the belly and curved the body. (d–f) The liver phenotypes in dissected males. Hepatic ulcers (black arrow) were observed in the beclin1+/− males. (g–i) H&E histological assay showing the tumor cells cords and bile sequestrations (black arrow) in beclin1+/−. (C) (a–c) Representative pictures of 16-month-old male zebrafish. (d–f) The liver phenotypes in dissected males. beclin1+/− liver had a hemorrhagic and necrotic appearance distributed on the inferior surface of the liver (black arrow). (g–i) H&E histological assay showing the development of confocal necrosis at 16-month-old male beclin1+/− (black arrow). NC: Necrosis. (D) Prevalence of microscopic hepatocellular malignancy. n = 10 for each experimental group. (E) Meire Kaplan graphs depicting the survival rate of the three reared strains. n = 50 for each experimental group. Beclin1+/− exhibited lower survival rate than WT at 12- and 16-month-old respectively (p < 0.0001). L: liver, the dotted frame represents liver histology in the underlined pictures.