Downregulation of IL6 Targeted MiR-376b May Contribute to a Positive IL6 Feedback Loop During Early Liver Regeneration in Mice

Cell Physiol Biochem. 2015;37(1):233-42. doi: 10.1159/000430348. Epub 2015 Aug 20.

Abstract

Background/aims: MicroRNAs (miRNAs) are a group of endogenous, small, noncoding RNAs implicated in a variety of biological processes, including cell proliferation, apoptosis, differentiation and metabolism. The present study aims to explore the potential role and molecular mechanism of miR-376b during the early phase of liver regeneration.

Methods: MiRNA profiling microarrays were used to assess the changes in miRNA expression. For functional analysis, cell proliferation, apoptosis assays, real time quantitative PCR and westernblot analysis were performed.

Results: The comprehensive miRNA expression profiling assays on regenerating liver tissues 4 h after partial hepatectomy (PH) showed that three miRNAs (miR-127, miR-376b and miR-494) located in the Dlk1-Gtl2 miRNA cluster were significantly downregulated. In vitro functional studies demonstrated that high-level interleukin 6 (IL6) inhibited the expression of miR-376b, and miR-376b mimics treatment decreased cell proliferation and increased apoptosis. Further target analysis showed that miR-376b reduced the mRNA and protein expression levels of NF-kappa-B inhibitor zeta (NFKBIZ) and signal transducers and transcription activators 3 (STAT3). Additionally, IL6-induced miR-376b downregulation would, in turn, increase the expression of IL-6 possibly via a feedback loop involving NFKBIZ or/and STAT3.

Conclusion: During the early phase of liver regeneration, miR-376b expression was significantly decreased. Our findings reveal that a regulatory circuitry between miR-376b and IL-6 may exist, which trigger the initiation of liver regeneration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Animals
  • Apoptosis / genetics
  • Cell Differentiation / genetics
  • Cell Proliferation / genetics
  • Down-Regulation / genetics*
  • Feedback
  • Gene Expression Regulation / genetics
  • Interleukin-6 / genetics*
  • Liver Regeneration / genetics*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / genetics*
  • Nuclear Proteins / genetics
  • RNA, Messenger / genetics
  • STAT3 Transcription Factor / genetics
  • Signal Transduction / genetics

Substances

  • Adaptor Proteins, Signal Transducing
  • Interleukin-6
  • MicroRNAs
  • Nfkbiz protein, mouse
  • Nuclear Proteins
  • RNA, Messenger
  • STAT3 Transcription Factor