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Hepatocyte nuclear factor 4β protect zebrafish from dexamethasone-induced hepatobiliary syndrome and hepatobiliary syndrome complicated with GCRV-II infection by targeting Hsp70 and inhibiting autophagy

ABSTRACT: Hepatocyte nuclear factor 4β (Hnf4β), a nuclear receptor superfamily member, acts as a key regulator of functional gene expression and various cellular processes. The function of Hnf4β in metabolic diseases or infectious diseases had not yet defined in teleost. Here, we show that zebrafish Hnf4β plays a protective role in the host defense against dexamethasone (DEX)-induced hepatobiliary syndrome and hepatobiliary syndrome complicated with GCRV-II infection. Zebrafish Hnf4β deficiency have hepatomegaly, lipid deposition, impairs larvae survival and regulates the expression levels of many genes involved in oxidative phosphorylation and spliceosome during DEX treatment plus GCRV-II infection. In addition, Hnf4β gene disruption in zebrafish leads to induction of oxidative stress with the increased susceptibility to dexamethasone-induced hepatobiliary syndrome complicated with GCRV-II infection. Furthermore, we show that zebrafish Hsp70 promote the translocation of Hnf4β from the nucleus to the cytoplasm and interact with Hnf4β in the cytoplasm and nucleus at DEX + GCRV situation. Mechanistically, zebrafish Hnf4β mediates the beneficial effect for larvae survival and lipid metabolism in the case of DEX treatment plus GCRV-II infection is depending on the Hsp70-mediated autophagy. Collectively, our results identify that the mechanisms of zebrafish Hnf4β through targeting Hsp70 against dexamethasone-induced hepatobiliary syndrome complicated with GCRV-II infection.

ORGANISM(S): Danio rerio

PROVIDER: GSE303991 | GEO | 2026/01/01

REPOSITORIES: GEO

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