LncRNA NKILA upregulation mediates oxygen glucose deprivation/re-oxygenation-induced neuronal cell death by inhibiting NF-κB signaling

Biochemical and Biophysical Research Communications
Mei WangTao Jin

Abstract

Oxygen glucose deprivation (OGD)/re-oxygenation (OGDR) induces severe injury to neuronal cells. The expression and potential function of NKILA (NF-κB Interacting LncRNA) in OGDR-treated neuronal cells were tested in this study. We show that OGDR induced NKILA upregulation to in-activate NF-κB signaling in SH-SY5Y cells and primary murine hippocampal neurons. Conversely, shRNA-mediated NKILA silencing almost reversed OGDR-induced NF-κB inhibition. OGDR-induced neuronal cell viability reduction, apoptosis and necrosis were largely attenuated by NKILA shRNA as well. Conversely, ectopic overexpression of NKILA by a lentiviral vector enhanced OGDR-induced SH-SY5Y cell death. For the mechanism study, we show that OGDR downregulated miR-103 and miR-107 to induce NKILA upregulation in neuronal cells. Transfection of miR-103 mimic or miR-107 mimic almost reversed OGDR-induced NKILA upregulation, NF-κB in-activation and SH-SY5Y cell death. Taken together, OGDR induces NKILA upregulation to in-activate NF-κB signaling, which mediates subsequent neuronal cell death. NKILA could be a novel therapeutic target of ischemic neuronal injury.

Citations

Sep 1, 2020·Cellular and Molecular Neurobiology·Ziyu WangWeirong Fang
Nov 17, 2020·Frontiers in Aging Neuroscience·Junfen FanYumin Luo
Apr 28, 2021·Neurochemistry International·Jian ChenYun Xu
Jul 30, 2021·Scientific Reports·Jesús Eduardo Rojo Arias, József Jászai

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