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  • Title: Mutated IkappaBalpha represses proliferation of immortalized neural progenitor cells and prevents their apoptosis after oxygen-glucose deprivation.
    Author: Zhu C, Liu Z, Gui L, Yao W, Qian W, Zhang C.
    Journal: Brain Res; 2008 Dec 09; 1244():24-31. PubMed ID: 18773881.
    Abstract:
    Endogenic and transplanted neural progenitor cells (NPCs) can be activated by cerebral ischemia and take part in the regeneration of neural function. NF-kappaB was found activated in the same pathology procedure and was assumed to play a crucial role in regulating NPCs' physiology. But it is still not clear whether NF-kappaB is activated in NPCs in cerebral ischemia and what is the effect of NF-kappaB on NPCs when activated. Our previous work generated immortalized neural progenitor cells (INPCs) to provide simulation for NPCs. Then pcDNA3.1 transfected INPCs (INPCs/pcDNA3.1) and mutated IkappaBalpha gene transfected INPCs (INPCs/IkappaBalphaM) were generated. By western blotting and electrophoretic mobility shift assay mutated IkappaBalpha was found expressed in INPCs/IkappaBalphaM and repressed the activity of NF-kappaB in INPCs. No difference in the differentiation of INPCs/pcDNA3.1 and INPCs/IkappaBalphaM was found by western blotting and immunocytochemistry. Detected by MTT assay INPCs/IkappaBalphaM had a lower proliferation rate under normal conditions. The apoptosis rate and lactate dehydrogenase activity in the medium of INPCs/IkappaBalphaM were lower than INPCs/pcDNA3.1 after oxygen-glucose deprivation. Some NF-kappaB-driven cytokines were observed down-regulated in INPCs/IkappaBalphaM by real-time reverse transcription polymerase chain reaction. In our research NF-kappaB was found activated in INPCs after oxygen-glucose deprivation. NF-kappaB activity down-regulation represses proliferation of INPCs and improves their tolerance to oxygen-glucose deprivation.
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