ArticleDevelopment (Cambridge, England)2025
Khdrbs1 drives re-differentiation of bipotential progenitor cells by inhibiting p53 in zebrafish biliary-mediated liver regeneration.
Article in Development (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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7 authors.
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Abstract
After severe liver injury, biliary epithelial cells (BECs) undergo de-differentiation into bipotential progenitor cells (BPPCs), which subsequently re-differentiate into nascent hepatocytes and BECs to accomplish liver regeneration. However, the crucial factors governing the re-differentiation process of BPPCs remain largely unknown. Here, using a zebrafish model of severe liver injury, we observed specific expression of khdrbs1a and khdrbs1b (collectively known as khdrbs1) in BPPCs through single-cell RNA analyses and fluorescence in situ hybridization. Subsequently, to eliminate the genetic compensation, we generated a CRISPR/dead Cas9-mediated system for interfering with khdrbs1 in BECs, which caused defective liver regeneration and impaired re-differentiation of BPPCs. Furthermore, the khdrbs1-/- mutant displayed impaired proliferation and re-differentiation of BPPCs during liver regeneration. Mechanistically, p53 signaling was activated in response to the loss of khdrbs1, and tp53 mutation partially rescued the defective liver regeneration of the khdrbs1-/- mutant. In summary, we conclude that Khdrbs1 promotes the re-differentiation of BPPCs in part by inhibiting p53 activation during biliary-mediated liver regeneration in zebrafish.
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