scholarly journals Deletion of TRPC6 Attenuates NMDA Receptor-Mediated Ca2+ Entry and Ca2+-Induced Neurotoxicity Following Cerebral Ischemia and Oxygen-Glucose Deprivation

2017 ◽  
Vol 11 ◽  
Author(s):  
Jin Chen ◽  
Zhaozhong Li ◽  
Jeffery T. Hatcher ◽  
Qing-Hui Chen ◽  
Li Chen ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals SUMO2/3 Conjugation is an Endogenous Neuroprotective Mechanism

2011 ◽  
Vol 31 (11) ◽  
pp. 2152-2159 ◽  
Author(s):  
Anna Lena Datwyler ◽  
Gisela Lättig-Tünnemann ◽  
Wei Yang ◽  
Wulf Paschen ◽  
Sabrina Lin Lin Lee ◽  
...  
Keyword(s):  
Stress Response ◽  
Cerebral Ischemia ◽  
Cortical Neurons ◽  
Neuronal Loss ◽  
Glucose Deprivation ◽  
Transient Cerebral Ischemia ◽  
Oxygen Glucose Deprivation ◽  
Primary Cortical Neurons ◽  
Microrna Delivery

Small ubiquitin-like modifier (SUMO)2/3 but not SUMO1 conjugation is activated after transient cerebral ischemia. To investigate its function, we blocked neuronal SUMO2/3 translation through lentiviral microRNA delivery in primary cortical neurons. Viability was unaffected by SUMO2/3 silencing unless neurons were stressed by transient oxygen–glucose deprivation (OGD). Both 15 and 45 minutes of OGD were tolerated by control microRNA-expressing neurons but damaged >60% of neurons expressing SUMO2/3 microRNA. Damaging OGD (75 minutes) increased neuronal loss to 54% (control microRNA) and to 99% (SUMO2/3 microRNA). This suggests that activation of SUMO2/3 conjugation is an endogenous neuroprotective stress response.

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