Gα₁₂ overexpression induced by miR-16 dysregulation contributes to liver fibrosis by promoting autophagy in hepatic stellate cells.

ABSTRACT:

Background & aims

Hepatic stellate cells (HSCs) have a role in liver fibrosis. Guanine nucleotide-binding α-subunit 12 (Gα₁₂) converges signals from G-protein-coupled receptors whose ligand levels are elevated in the environment during liver fibrosis; however, information is lacking on the effect of Gα₁₂ on HSC trans-differentiation. This study investigated the expression of Gα₁₂ in HSCs and the molecular basis of the effects of its expression on liver fibrosis.

Methods

Gα₁₂ expression was assessed by immunostaining, and immunoblot analyses of mouse fibrotic liver tissues and primary HSCs. The role of Gα₁₂ in liver fibrosis was estimated using a toxicant injury mouse model with Gα₁₂ gene knockout and/or HSC-sp

SUBMITTER: Kim KM 

PROVIDER: S-EPMC5818314 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature