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microRNA‐146a is involved in rSjP40‐inhibited activation of LX‐2 cells by targeting Smad4 expression
Author(s) -
Zhu Dandan,
Hu Bin,
Zhou Yonghua,
Sun Xiaolei,
Chen Jinling,
Chen Liuting,
Ji Zhaodong,
Zhu Jinhua,
Duan Yig
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27193
Subject(s) - hepatic stellate cell , microrna , schistosoma japonicum , microbiology and biotechnology , hepatic fibrosis , chemistry , signal transduction , transfection , downregulation and upregulation , fibrosis , biology , cancer research , immunology , biochemistry , gene , medicine , pathology , endocrinology , schistosomiasis , helminths
Abstract Previous studies have demonstrated that the recombinant Schistosoma japonicum protein P40 (rSjP40) could inhibit activation of hepatic stellate cells (HSCs) through the TGF‐β1/Smads signaling pathway. Since multiple microRNAs could play essential roles in HSC activation and in the process of hepatic fibrosis through targeting Smads, we attempted to seek the potential microRNAs that could be involved in rSjP40‐induced inhibition of HSC activation. Using the method of quantitative real‐time PCR, we found that rSjP40 could induce miR‐146a expression in LX‐2 cells. The down‐regulated expression levels of Smad4 and α‐SMA in LX‐2 cells induced by rSjP40 were partially restored by an miR‐146a inhibitor. miR‐146a can be involved in rSjP40‐induced inhibition of HSC activation through targeting Smad4. These findings provide us a new idea to explore the potential mechanisms by which rSjP40 could regulate the process of hepatic fibrosis.