Effects of calprotectin S100A8/A9 on primary hepatic stellate cells of mice based on quantitative proteomics
10.7644/j.issn.1674-9960.2025.10.001
- VernacularTitle:钙卫蛋白S100A8/A9对原代小鼠肝星状细胞激活效应的定量蛋白质组学研究
- Author:
Ruixi LIU
1
;
Jinfang LIU
;
Jian WANG
;
Ping XU
Author Information
1. 军事科学院军事医学研究院,医学蛋白质组学全国重点实验室,北京蛋白质组研究中心,国家蛋白质科学中心(北京),北京 102206
- Keywords:
calprotectin S100A8/A9;
hepatic stellate cells;
quantitative proteomics;
liver fibrosis
- From:
Military Medical Sciences
2025;49(10):721-727
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the direct stimulatory effects of calprotectin S100A8/A9 on hepatic stellate cells(HSCs)and underlying regulatory mechanisms.Methods Primary HSCs of mice were stimulated with S100A8/A9 heterodimer recombinant protein at 200 and 1000 ng/mL.Data on quantitative proteomics was obtained using the tandem mass tag(TMT)-labeled method before changes in the protein level of HSCs were analyzed.Differentially expressed proteins(DEPs)were screened using Significance B method and P＜0.05,followed by Reactome pathway enrichment analysis.Furthermore,protein-protein interactions between the DEPs enriched in the pathways were analyzed using the STRING database.Results The protein expression profile of HSCs was significantly altered after treatment with S100A8/A9 at 1000 ng/mL.Reactome pathway enrichment analysis revealed significant enrichment in such pathways as transforming growth factor-beta(TGF-β)signaling,nuclear factor kappa-B(NF-κB)signaling activation,cytokine-mediated immune regulation,and collagen biosynthesis.The analysis of protein-protein interactions identified NF-kappa-B transcription factor subunit(RELB),chemokine(C-X-C motif)ligand 10(CXCL10)and Notch receptor 1(NOTCH1)as key hub proteins in the regulatory network.Conclusion S100A8/A9 can directly stimulate the activation of HSCs,through NF-κB signaling,TGF-β signaling,and Notch signaling pathways potentially.This study sheds light on the mechanisms underlying the activation of HSCs stimulated by S100A8/A9.
