Changes in microRNA expression in response to <i>Schistosoma japonicum</i> infection

Hong, Yang; Fu, Zhiqiang; Cao, Xiaodan; Lin, Jiaojiao

doi:10.1111/pim.12416

Cited by 15 publications

(14 citation statements)

References 66 publications

(140 reference statements)

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“…9 Moreover, microRNA-143 also plays an important role in infectious liver disease like hepatitis B, 10,11 hepatitis C 12 and/or Schistosoma japonicum. 13 Although the mechanisms underlying these effects are not fully known, several studies have shown involvement of sprouty3 (SPRY3) 7 and Akt/mTOR pathway 8 in miRNA regulation of gene expression.…”

Section: Introductionmentioning

confidence: 99%

microRNA‐143‐3p attenuated development of hepatic fibrosis in autoimmune hepatitis through regulation of TAK1 phosphorylation

Chen

Cai

et al. 2019

J Cellular Molecular Medi

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Autoimmune hepatitis (AIH) is a chronic liver disease due to autoimmune system attacks hepatocytes and causes inflammation and fibrosis. Intracellular signalling and miRNA may play an important role in regulation of liver injury. This study aimed to investigate the potential roles of microRNA 143 in a murine AIH model and a hepatocyte injury model. Murine AIH model was induced by hepatic antigen S100, and hepatocyte injury model was induced by LPS. Mice and AML12 cells were separated into six groups with or without the treatment of miRNA-143. Inflammation and fibrosis as well as gene expression were examined by different cellular and molecular techniques. The model was successfully established with the elevation of ALT and AST as well as inflammatory and fibrotic markers. Infection or transfection of mir-143 in mice or hepatocytes significantly attenuated the development of alleviation of hepatocyte injury. Moreover, the study demonstrated phosphorylation of TAK1-mediated miRNA-143 regulation of hepatic inflammation and fibrosis as well as hepatocyte injury. Our studies demonstrated a significant role of miRNA-143 in attenuation of liver injury in AIH mice and hepatocytes. miRNA-143 regulates inflammation and fibrosis through its regulation of TAK1 phosphorylation, which warrants TAK1 as a target for the development of new therapeutic strategy of autoimmune hepatitis. K E Y W O R D S autoimmune hepatitis, gene therapy, liver fibrosis, miR-143, TAK1 | 1257 TU eT al.

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Section: Introductionmentioning

confidence: 99%

microRNA‐143‐3p attenuated development of hepatic fibrosis in autoimmune hepatitis through regulation of TAK1 phosphorylation

Chen

Cai

et al. 2019

J Cellular Molecular Medi

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“…Dai et al have also demonstrated that inhibition of miR‐155 expression may induce HSC activation through ERK1 pathway. Which is more important, Cai et al also reported that miR‐155 exhibited a peak in the liver of mice infected with Schistosoma japonicum and Hong et al have concluded that miR‐155 may be involved in the regulation of hepatic inflammatory responses and the development of schistosomal hepatopathy. In this study, we observed that miR‐155 expression increased in rSjP40‐treated LX‐2 cells (Figure ).…”

Section: Discussionmentioning

confidence: 99%

rSjP40 suppresses hepatic stellate cell activation by promoting microRNA‐155 expression and inhibiting STAT5 and FOXO3a expression

Zhu

Yang

Shen

et al. 2018

J Cellular Molecular Medi

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Activation of hepatic stellate cells (HSCs) is the central event of the evolution of hepatic fibrosis. Schistosomiasis is one of the pathogenic factors which could induce hepatic fibrosis. Previous studies have shown that recombinant Schistosoma japonicum egg antigen P40 (rSjP40) can inhibit the activation and proliferation of HSCs. MicroRNA‐155 is one of the multifunctional noncoding RNA, which is involved in a series of important biological processes including cell development, proliferation, differentiation and apoptosis. Here, we try to observe the role of microRNA‐155 in rSjP40‐inhibited HSC activation and explore its potential mechanisms. We found that microRNA‐155 was raised in rSjP40‐treated HSCs, and further studies have shown that rSjP40 enhanced microRNA‐155 expression by inhibiting STAT5 transcription. Up‐regulated microRNA‐155 can down‐regulate the expression of FOXO3a and then participate in rSjP40‐inhibited expression of α‐smooth muscle actin (α‐SMA) and collagen I. Furthermore, we observed microRNA‐155 inhibitor could partially restore the down‐regulation of FOXO3a, α‐SMA and collagen I expression in LX‐2 cells induced by rSjP40. Therefore, our research provides further insight into the mechanism by which rSjP40 could inhibit HSC activation via miR‐155.

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“…Identifying changes in miRNA profile in response to parasite infections and the networks these miRNAs regulate is highly informative in explaining immunopathology and may lead to novel therapies to reduce these effects. Mir‐155 and mir‐146 were also among the miRNAs upregulated in the liver following infection with the human‐infective trematode Schistosoma japonicum and, as reviewed by Hong et al., may regulate the inflammatory and T‐ and B‐cell responses to schistosome egg antigens. Several miRNAs have been associated with regulation of hepatic fibrosis, and future studies aimed at testing the effects of mimics of these will be important in determining their potential therapeutic value in reducing liver pathology.…”

Section: Mirna Regulation May Contribute To Immunopathology Of Parasimentioning

confidence: 99%

microRNAs—key players in host–parasite interactions

Britton

2017

Parasite Immunology

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Changes in microRNA expression in response to Schistosoma japonicum infection

Cited by 15 publications

References 66 publications

microRNA‐143‐3p attenuated development of hepatic fibrosis in autoimmune hepatitis through regulation of TAK1 phosphorylation

microRNA‐143‐3p attenuated development of hepatic fibrosis in autoimmune hepatitis through regulation of TAK1 phosphorylation

rSjP40 suppresses hepatic stellate cell activation by promoting microRNA‐155 expression and inhibiting STAT5 and FOXO3a expression

microRNAs—key players in host–parasite interactions

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