Recombinant truncated latency-associated peptide alleviates liver fibrosis in vitro and in vivo via inhibition of TGF-β/Smad pathway.

ABSTRACT:

Background

Liver fibrosis is a progressive liver injury response. Transforming growth factor β1 (TGF-β1) is oversecreted during liver fibrosis and promotes the development of liver fibrosis. Therapeutic approaches targeting TGF-β1 and its downstream pathways are essential to inhibit liver fibrosis. The N-terminal latency-associated peptide (LAP) blocks the binding of TGF-β1 to its receptor. Removal of LAP is critical for the activation of TGF-β1. Therefore, inhibition of TGF-β1 and its downstream pathways by LAP may be a potential approach to affect liver fibrosis.

Methods

Truncated LAP (tLAP) plasmids were constructed. Recombinant proteins were purified by Ni affinity chromatography. The effects of LAP and tLAP on liver fibrosis were investigated in TGF-β1-induced HSC-T6 ce

SUBMITTER: Song X 

PROVIDER: S-EPMC9288003 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature