Interleukin-26 promotes the proliferation and activation of hepatic stellate cells to exacerbate liver fibrosis by the TGF-β1/Smad2 signaling pathway.
Year: 2019
Type: article
Abstract: . By cell counting kit (CCK)-8 assay, we observed that IL-26 significantly promoted the proliferation of HSCs by increasing S phase and decreasing G0/G1 phase. Annexin V-FITC/PI double staining showed that IL-26 could suppress the apoptosis of HSCs by inhibition of caspase 3 (CASP3) and Bcl-2 associated X protein (BAX). Furthermore, quantitative real-time PCR (qRT-PCR) assay and western blotting analysis revealed that IL-26 exacerbated the degree of hepatic fibrosis, which was associated with the upregulation of the mRNA levels and protein concentrations of IL-6, IL-10, tumor necrosis factor (TNF)-α, matrix metallopeptidase (MMP)-9, and α-smooth muscle act in (SMA). Mechanistically, western blotting analysis showed that IL-26 upregulated the protein expression levels of transforming growth factor (TGF)-β1 and SMAD family member 2 (Smad2) in HSCs. In summary, the data demonstrated a key role of IL-26 on the proliferation and activation of HSCs in liver fibrosis and the underlying mechanism might be related to the TGF-β1/Smad2 signaling pathway. The finding will provide a proof that targeting IL-26 may be developed as therapeutics for liver fibrosis.
Source: PubMed
Authors: Xinqi Zhang, Xiaoye Xie, Yanzhao Wang, Wenfang Li, Zhaofen Lin
Language: English
Subfield: Hepatology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W3011231436