Hepatocyte-derived Pumilio1-enriched exosomes inhibit HSC activation by suppressing tropomyosin-4 translation.

ABSTRACT:

Background

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most common chronic liver disease globally. Abnormal crosstalk between hepatocytes and HSCs leads to liver fibrosis and aggravates MASLD. We explored the role of the RNA-binding protein Pumilio in this process.

Methods

Two isoforms of Pumilio proteins (PUM1, PUM2) expression were analyzed in the livers of MASLD patients and mice. MASLD mice were induced by a western diet combined with intraperitoneal injection of carbon tetrachloride (WD+CCl4), or a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). Adeno-associated virus type 8 carrying Pum1-targeting short hairpin RNA or small interfering RNA targeting PUM1 was used to knock down PUM1 in vivo or in vitro. Ultracentrifug

SUBMITTER: Wan Z 

PROVIDER: S-EPMC12263002 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature