Reciprocal induction of hepatitis C virus replication and stimulation of hepatic profibrogenic cytokine release and cellular viability by YKL-40.

ABSTRACT:

Background

Previous studies have suggested the YKL-40/chitinase 3-like protein 1 protein is upregulated in chronic hepatitis C virus (HCV) infection with fibrosis. We sought to determine whether HCV regulates YKL-40 expression and to elucidate the mechanisms by which YKL-40 mediates the liver fibrosis caused by HCV infection.

Methods

We used purified protein, small molecule inhibitors and short-interfering RNAs to over-express or knock down certain kinases to explore the mechanisms underlying the regulation by HCV of YKL-40 expression in the Japanese fulminant hepatitis 1 (JFH1) model.

Results

HCV induced YKL-40 production in hepatic parenchymal cells. Further, HCV-mediated upregulation of YKL-40 through cooperative induction of tumor necrosis factor-α (TNF-α) and rea

SUBMITTER: Cheng D 

PROVIDER: S-EPMC8667091 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature