Regulation of programmed cell death in neuronal cells by nitric oxide

Yun Chul Kang, Peter K. Kim, Byoung Min Choi, Hun Taeg Chung, Kwon Soo Ha, Young Guen Kwon, Young Myeong Kim

Research output: Contribution to journalReview articlepeer-review

45 Citations (Scopus)


Nitric oxide (NO), produced from L-arginine and molecular oxygen in a reaction catalyzed by one of three NO synthase isoenzymes, can prevent or induce neuronal apoptosis depending on its concentration and cellular redox state. This molecule affords neuroprotection by post-translational-S-nitrosylation of NMDA receptor, caspases and p21ras, and increases the expression of cytoprotective genes such as HSP70, heme oxygenase and Bcl-2. Moreover, the NO/cGMP pathway activates the anti-apoptotic serine/threonine kinase Akt by protein kinase G-dependent activation of phosphatidylinositol 3-kinase. A high concentration of NO and peroxynitrite, a reaction product of NO with superoxide anion, can promote apoptotic pathways in neuronal cells through the indirect activation of caspases. We review the molecular mechanism by which NO exerts both pro- and anti-apoptotic actions in neuronal cells and the clinical implications for regulating neuronal apoptos.

Original languageEnglish
Pages (from-to)367-376
Number of pages10
JournalIn Vivo
Issue number3
Publication statusPublished - 2004

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology


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