Hypoxia induces the activation of hepatic stellate cells through the PVT1-miR-152-ATG14 signaling pathway

Mol Cell Biochem. 2020 Feb;465(1-2):115-123. doi: 10.1007/s11010-019-03672-y. Epub 2019 Dec 21.

Abstract

Increasing studies have indicated that hypoxia serves as a pivotal microenvironmental factor that facilitates activation of hepatic stellate cells (HSCs). However, the mechanism by which hypoxia activates HSCs is not clear. Here, we demonstrated that plasmacytoma variant translocation 1 (PVT1) and autophagy were overexpressed in liver fibrotic specimens. In primary mouse HSCs, both PVT1 and autophagy were induced by hypoxia. Further study showed that hypoxia-induced autophagy depended on expression of PVT1 and miR-152 in HSCs. Luciferase reporter assay indicated that autophagy-related gene 14 (ATG14) was a direct target of miR-152. In addition, inhibition of autophagy by 3-methyladenine and Beclin-1 siRNA impeded activation of HSCs cultured in 1% O2. Taken together, autophagy induction via the PVT1-miR-152-ATG14 signaling pathway contributes to activation of HSCs under hypoxia condition.

Keywords: Autophagy; Hepatic stellate cell; Hypoxia; Plasmacytoma variant translocation 1 (PVT1); microRNA-152.

MeSH terms

  • Animals
  • Autophagic Cell Death*
  • Autophagy-Related Proteins / metabolism*
  • Cell Hypoxia
  • Hepatic Stellate Cells / metabolism*
  • Hepatic Stellate Cells / pathology
  • Liver Cirrhosis / metabolism
  • Liver Cirrhosis / pathology
  • Mice
  • MicroRNAs / metabolism*
  • RNA, Long Noncoding / metabolism*
  • Signal Transduction*
  • Vesicular Transport Proteins / metabolism*

Substances

  • Atg14 protein, mouse
  • Autophagy-Related Proteins
  • MIRN152 microRNA, mouse
  • MicroRNAs
  • PVT1 long-non-coding RNA, mouse
  • RNA, Long Noncoding
  • Vesicular Transport Proteins