LncRNA NKILA upregulation mediates oxygen glucose deprivation/re-oxygenation-induced neuronal cell death by inhibiting NF-κB signaling
- Department of Hepatobiliary Surgery, The Second Affiliated Hospital, Mudanjiang College of Medicine, Mudanjiang (China)
- Department of Ophthalmology, The Second Affiliated Hospital, Mudanjiang College of Medicine, Mudanjiang (China)
- Department of Neurosurgery, The Second Affiliated Hospital, Mudanjiang College of Medicine, Mudanjiang (China)
- Department of Anatomy, Mudanjiang College of Medicine, Mudanjiang (China)
Highlights: • OGDR induces NKILA expression to inhibit NF-κB activation in neuronal cells. • NKILA shRNA attenuates OGDR-induced NF-κB inhibition and neuronal cell death. • NKILA overexpression augments OGDR-induced neuronal cell death. • miR-103/107 downregulation mediates NKILA upregulation by OGDR in neuronal cells. 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.
- OSTI ID:
- 23134249
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 503; ISSN 0006-291X; ISSN BBRCA9
- Country of Publication:
- United States
- Language:
- English
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