Nuclear shrinkage and other markers of neuronal cell death after oxygen–glucose deprivation in rat hippocampal slice cultures

2002 ◽  
Vol 327 (1) ◽  
pp. 49-52 ◽  
Author(s):  
Christian Bonde ◽  
Jens Noraberg ◽  
Jens Zimmer
2016 ◽  
Vol 223 (4) ◽  
pp. S82 ◽  
Author(s):  
Vahagn C. Nikolian ◽  
Peter J. Bruhn ◽  
Patrick E. Georgoff ◽  
Ihab Halaweish ◽  
Baihong Pan ◽  
...  

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Shu Xu ◽  
Ya Li ◽  
Ju-ping Chen ◽  
Da-Zhuang Li ◽  
Qin Jiang ◽  
...  

Abstract Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. In SH-SY5Y cells and primary murine neurons, we report that OGD/R induces the accumulation of the microRNA miR-422a, leading to downregulation of miR-422a targets myocyte enhancer factor-2D (MEF2D) and mitogen-activated protein kinase kinase 6 (MAPKK6). Ectopic miR-422a inhibition attenuated OGD/R-induced cell death and apoptosis, whereas overexpression of miR-422a induced significant neuronal cell apoptosis. In addition, OGD/R decreased the expression of the long non-coding RNA D63785 (Lnc-D63785) to regulate miR-422a accumulation. Lnc-D63785 directly associated with miR-422a and overexpression of Lnc-D63785 reversed OGD/R-induced miR-422a accumulation and neuronal cell death. OGD/R downregulated Lnc-D63785 expression through increased methyltransferase-like protein 3 (METTL3)-dependent Lnc-D63785 m6A methylation. Conversely METTL3 shRNA reversed OGD/R-induced Lnc-D63785 m6A methylation to decrease miR-422a accumulation. Together, Lnc-D63785 m6A methylation by OGD/R causes miR-422a accumulation and neuronal cell apoptosis.


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