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rSjP40 protein promotes PPARγ expression in LX-2 cells through microRNA-27b

Dandan Zhu1, Lei Lyu1,2, Pei Shen3

  • 1Department of Pathogen Biology, School of Medicine, Nantong University, Nantong, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 3, 2018
PubMed

Insights

The recombinant P40 protein from Schistosoma japonicum (rSjP40) inhibits hepatic stellate cell activation by down-regulating microRNA-27b (miR-27b) expression. This process involves miR-27b targeting peroxisome proliferator-activated receptor γ (PPARγ), offering insights into liver fibrosis mechanisms.

Area of Science:

  • Molecular Biology
  • Hepatology
  • Parasitology

Background:

  • Hepatic stellate cells (HSCs) play a crucial role in liver fibrosis.
  • MicroRNA-27b (miR-27b) is implicated in HSC proliferation, differentiation, and fat metabolism.
  • The recombinant P40 protein from Schistosoma japonicum (rSjP40) has shown potential in inhibiting HSC activation.

Purpose of the Study:

  • To investigate the effect of rSjP40 on miR-27b expression in LX-2 cells (a human HSC cell line).
  • To elucidate the underlying mechanisms of rSjP40's action on HSCs, focusing on miR-27b and its targets.
  • To explore the role of miR-27b methylation in rSjP40-mediated effects.

Main Methods:

  • Quantitative real-time PCR to measure miR-27b expression.
  • Western blot and dual-luciferase reporter assay to assess PPARγ regulation by miR-27b.
  • Treatment with 5-AZA-2'-deoxycytidine (5-AZA-dC) to investigate the role of DNA methylation.

Main Results:

  • rSjP40 significantly inhibited miR-27b expression in LX-2 cells.
  • miR-27b was confirmed to target the 3'-UTR of peroxisome proliferator-activated receptor γ (PPARγ), regulating its expression.
  • 5-AZA-dC partially reversed the effects of rSjP40 on both miR-27b and PPARγ expression, suggesting a role for methylation.

Conclusions:

  • rSjP40 inhibits HSC activation, at least partly, by down-regulating miR-27b expression.
  • The observed increase in PPARγ in rSjP40-treated cells may be mediated by reduced miR-27b levels and potentially influenced by methylation.
  • These findings provide a deeper understanding of rSjP40's mechanism in combating liver fibrosis.
Keywords:
Schistosoma japonicumhepatic stellate cellmethylationmiR-27b

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