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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
Published on: July 26, 2017
The role of TLR9 in stress-dependent autophagy formation
Jae Sung Lim1, Hyeon Sik Kim2, Kim Cuc Thi Nguyen1
1Department of Biochemistry, Chonnam National University Medical School, Gwangju 501-746, South Korea; Center for Creative Biomedical Scientists, Chonnam National University Medical School, Gwangju 501-746, South Korea.
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.
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