期刊
PARASITOLOGY RESEARCH
卷 118, 期 2, 页码 551-557出版社
SPRINGER
DOI: 10.1007/s00436-018-6165-3
关键词
Hepatic fibrosis; Hepatic stellate cell; IL-34; NF-kappa B
类别
资金
- National Natural Science Foundation of China [81871677, 81471975]
- Jiangsu Planned Projects for Postdoctoral Research Funds [1701170B]
- Priority Academic Program Development of Jiangsu Higher Education Institution (PAPD)
Hepatic fibrosis is characterized by the activation of the main collagen-producing cells of the liver, hepatic stellate cells, and is associated with inflammation. Although the involvement of numerous inflammatory cytokines has been reported, IL-34 in particular has recently been identified as a profibrotic factor in the development of hepatic fibrosis. Previous studies have found that schistosome eggs can lead to transcriptional downregulation of fibrosis-associated genes, and based on this evidence, we attempted to investigate whether or not IL-34 is regulated by soluble egg antigen (SEA). Our findings testified that SEA inhibited TNF--induced expression of IL-34 at both the mRNA and protein levels. Furthermore, results from reporter assays and qPCR experiments demonstrated that SEA impaired the activation of NF-B triggered by TNF-, as well as the transcription of downstream genes. More importantly, SEA decreased the phosphorylation and degradation of IB induced by TNF-, two events that are hallmarks of canonical NF-B activation. In conclusion, our results suggest that, in hepatic stellate cells, SEA impairs NF-B activation and thereby inhibits TNF--induced IL-34 expression. These findings reveal a previously unidentified target and signaling pathway that support SEA's involvement in hepatic fibrosis and provide a new clue to guide ongoing research into the anti-fibrotic effects of SEA.
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