Study on pathophysiological roles of brain NO-NCX signal

点击翻译按钮获取中文摘要

This study examined the role of the predominant brain-specific NCX splice variant NCX1.5 in NO-induced cytotoxicity in HEK293 cell expression system. Transfection with a plasmid construct pcDNA3.1/V5-His containing full-length rat NCX1.5 cDNA into HEK293 cells increased prominently the protein level of NCX1.5 tagged with C-terminal V5 and (His)6 epitopes (NCX1.5-V5/His). There was no difference in the cytotoxic effects by sodium nitroprusside and S-nitroso-N-acetylpenicillamine between the control and transfected cells. These results suggest that NO cytotoxicity is not dependent on NCX1.5. Microdialysis study showed that NO did not affect monoamine release in the brain. Furthermore, RT-PCR analysis showed that environmental factors did not affect the expression of NCX.