Mutated IκBα represses proliferation of immortalized neural progenitor cells and prevents their apoptosis after oxygen–glucose deprivation

Endogenic and transplanted neural progenitor cells (NPCs) can be activated by cerebral ischemia and take part in the regeneration of neural function. NF-κB 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-κB is activated in NPCs in cerebral ischemia and what is the effect of NF-κB 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 IκBα gene transfected INPCs (INPCs/IκBαM) were generated. By western blotting and electrophoretic mobility shift assay mutated IκBα was found expressed in INPCs/IκBαM and repressed the activity of NF-κB in INPCs. No difference in the differentiation of INPCs/pcDNA3.1 and INPCs/IκBαM was found by western blotting and immunocytochemistry. Detected by MTT assay INPCs/IκBαM had a lower proliferation rate under normal conditions. The apoptosis rate and lactate dehydrogenase activity in the medium of INPCs/IκBαM were lower than INPCs/pcDNA3.1 after oxygen–glucose deprivation. Some NF-κB-driven cytokines were observed down-regulated in INPCs/IκBαM by real-time reverse transcription polymerase chain reaction. In our research NF-κB was found activated in INPCs after oxygen–glucose deprivation. NF-κB activity down-regulation represses proliferation of INPCs and improves their tolerance to oxygen–glucose deprivation.