Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 502, Issue 1, Pages 166-172Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.05.141
Keywords
Neuroligin-3; Retinal cells; Oxidative stress; Nrf2; AktmTORC1; Signaling
Categories
Funding
- National Natural Science Foundation of China [81371055, 81570859, 81670878, 81700859]
- Medical Science and Technology Development Project Fund of Nanjing [YKK16271, YKK14193, YKK15241, YKK16269, YKK16270]
- Natural Science Foundation of Jiangsu Province [BK20161568]
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Intensified oxidative stress can cause severe damage to human retinal pigment epithelium (RPE) cells and retinal ganglion cells (RGCs). The potential effect of neuroligin-3 (NLGN3) against the process is studied here. Our results show that NLGN3 efficiently inhibited hydrogen peroxide (H2O2)-induced death and apoptosis in human RPE cells and RGCs. H2O2-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage in retinal cells were alleviated by NLGN3. NLGN3 activated nuclearfactor-E2-related factor 2 (Nrf2) signaling, enabling Nrf2 protein stabilization, nuclear translocation and expression of key anti-oxidant enzymes (HO1, NOQ1 and GCLC) in RPE cells and RGCs. Further results demonstrate that NLGN3 activated Akt-mTORC1 signaling in retinal cells. Conversely, Akt-mTORC1 inhibitors (RAD001 and LY294002) reduced NLGN3-induced HO1, NOQ1 and GCLC mRNA expression. Significantly, Nrf2 silencing by targeted shRNAs reversed NLGN3-induced retinal cytoprotection against H(2)O(2.)We conclude that NLGN3 activates Nrf2 signaling to protect human retinal cells from H2O2. NLGN3 could be further tested as a valuable retinal protection agent. (C) 2018 Elsevier Inc. All rights reserved.
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