The role of TLR9 in stress-dependent autophagy formation

Biochem Biophys Res Commun. 2016 Dec 9;481(3-4):219-226. doi: 10.1016/j.bbrc.2016.10.105. Epub 2016 Oct 26.

Abstract

Autophagy is a self-degradation process that is important for balancing energy sources at critical times in development and in response to nutrient stress. Recently, it was report that autophagy is controlled by recognizing conserved pattern recognition receptors (PRRs), including toll-like receptors (TLRs). However, the molecular mechanism of TLRs in autophagy is not well understood. In this study, we found that serum starvation-dependent autophagy was associated with TLR9 activation in the absence of CpG-ODN, which is a specific TLR9 ligand. TLR9 was not only elevated but also colocalized with LC3 during autophagy by serum starvation or CPG-ODN treatment; however, these events did not occur simultaneously during autophagosome accumulation. Autophagy was even induced upon TLR9 activation after inhibiting recruitment of initial autophagy components by 3-MA, a specific inhibitor of class III PI3-kinase. Our data suggested that TLR9 may be promptly induced and recruit autophagy components from the endosome to autophagosome in response to stress.

Keywords: Autophagy; Serum starvation; TLR9.

MeSH terms

  • Autophagy* / drug effects
  • Cell Compartmentation / drug effects
  • Culture Media, Serum-Free
  • Endosomes / drug effects
  • Endosomes / metabolism
  • HeLa Cells
  • Humans
  • Oligodeoxyribonucleotides / pharmacology
  • Phagosomes / drug effects
  • Phagosomes / metabolism
  • Stress, Physiological* / drug effects
  • Toll-Like Receptor 9 / metabolism*

Substances

  • CPG-oligonucleotide
  • Culture Media, Serum-Free
  • Oligodeoxyribonucleotides
  • Toll-Like Receptor 9