Role of Bcl-2 family of proteins in mediating apoptotic death of PC12 cells exposed to oxygen and glucose deprivation

2005 ◽  
Vol 46 (1) ◽  
pp. 73-81 ◽  
Author(s):  
D KOUBI ◽  
H JIANG ◽  
L ZHANG ◽  
W TANG ◽  
J KUO ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Apoptotic Death

Postconditioning mitigates cell death following oxygen and glucose deprivation in PC12 cells and forebrain reperfusion injury in rats

2014 ◽  
Vol 93 (1) ◽  
pp. 140-148 ◽  
Author(s):  
Han-Chen Lin ◽  
Purnima Narasimhan ◽  
Shin-Yun Liu ◽  
Pak H. Chan ◽  
I-Rue Lai
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation

scholarly journals A Concerted Role of Na+—K+—Cl− Cotransporter and Na+/Ca2+ Exchanger in Ischemic Damage

2007 ◽  
Vol 28 (4) ◽  
pp. 737-746 ◽  
Author(s):  
Jing Luo ◽  
Yanping Wang ◽  
Hai Chen ◽  
Douglas B Kintner ◽  
Sam W Cramer ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Mortality Rate ◽  
Neuronal Death ◽  
Cortical Neurons ◽  
Infarct Volume ◽  
Glucose Deprivation ◽  
Ischemic Damage ◽  
Oxygen And Glucose Deprivation

Na+–K+–Cl− cotransporter isoform 1 (NKCC1) and Na+/Ca2+ exchanger isoform 1 (NCX1) were expressed in cortical neurons. Three hours of oxygen and glucose deprivation (OGD) significantly increased expression of full-length NCX1 protein (∼116 kDa), which remained elevated during 1 to 21 h reoxygenation (REOX) and was accompanied with concurrent cleavage of NCX1. Na+/Ca2+ exchanger isoform 1 heterozygous (NCX1+/−) neurons with ∼50% less of NCX1 protein exhibited ∼64% reduction in NCX-mediated Ca2+ influx. Expression of NCX1 and NKCC1 proteins was reduced in double heterozygous (NCX1+/−/NKCC1+/−) neurons. NCX-mediated Ca2+ influx was nearly abolished in these neurons. Three-hour OGD and 21-h REOX caused ∼80% mortality rate in NCX1+/+ neurons and in NCX1+/− neurons. In contrast, NKCC1+/− neurons exhibited ∼45% less cell death. The lowest mortality rate was found in NCX1+/−/NKCC1+/− neurons (∼65% less neuronal death). The increased tolerance to ischemic damage was also observed in NCX1+/−/NKCC1+/− brains after transient cerebral ischemia. NCX1+/−/NKCC1+/− mice had a significantly reduced infarct volume at 24 and 72 h reperfusion. In conclusion, these data suggest that NKCC1 in conjunction with NCX1 plays a role in reperfusion-induced brain injury after ischemia.

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