Lentivirus-mediated over-expression of let-7b microRNA suppresses hepatic fibrosis in the mouse infected with Schistosoma japonicum.

Abstract:

:Transforming growth factor-β (TGF-β) signaling pathway is documented to participate in liver fibrosis via multifactorial mechanisms. microRNA Let-7b (Let-7b) has been proved to alleviate cell fibrosis through regulating TGF-β receptor I (TβRI), but whether it is involved in Schistosomiasis liver fibrosis (SLF) has not been determined. In the present, SLF mice model was used to investigate Let-7b's function and mechanism in SLF. We found that hepatic let-7b expression was continuously declined in SLF, accompanied by the induction of TGF-β pathway molecules (TGF-β1, TβRI), profibrogenic mediators (α-SMA, colla I), and Th1/Th2 cells response factors (IFN-γ, IL-4). When recombinant Lentivirus of let-7b (Lenti-let-7b) was transfected into S. japonicum-infected mice, the mice hepatic fibrosis was distinctly ameliorated, and TGF-β1, TβRI, α-SMA, and colla I expressions were remarkly decreased, mice serum IL-4 and IFN-γ levels were reduced. Similarly, over-expression of let-7b down-regulated the expression of TβRI in THP-1 cells transfected with let-7b mimics, while TβRI was up-regulated after treated with let-7b inhibitor. These findings suggested that let-7b is a negative regulator to SLF through downregulating TβRI, and inhibits Th1 and Th2 type cell immune response. This provides a novel potential therapeutic strategy for SFL prevention.

journal_name

Exp Parasitol

authors

Tang N,Wu Y,Cao W,Liang Y,Gao Y,Hu L,Yang Q,Zhou Y,Tang F,Xiao J

doi

10.1016/j.exppara.2017.09.024

subject

Has Abstract

pub_date

2017-11-01 00:00:00

pages

45-53

eissn

0014-4894

issn

1090-2449

pii

S0014-4894(17)30200-X

journal_volume

182

pub_type

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