Bax inhibitor-1 protects neurons from oxygen-glucose deprivation

J Mol Neurosci. 2006;29(1):1-8. doi: 10.1385/JMN:29:1:1.


Bax ihibitor-1 (BI-1) has been characterized as an inhibitor of Bax-induced cell death in plants and various mammalian cell systems. To explore the function of BI-1 in neurons, we overexpressed BI-1 tagged to HA or GFP in rat nigral CSM14.1 and human SH-SY5Y neuroblastoma cells. Stable BI-1 expression proved marked protection from cell death induced by thapsigargine, a stress agent blocking the Ca2+-ATPase of the endoplasmic reticulum (ER) but failed to inhibit cell death induced by staurosporine, a kinase inhibitor initiating mitochondria-dependent apoptosis. Moreover, BI-1 was neuroprotective in a paradigm mimicking ischemia, namely oxygen-glucose as well as serum deprivation. Examination of the subcellular distribution revealed that BI-1 predominantly locates to the ER and nuclear envelope but not mitochondria. Taken together, BI-1 overexpression in the ER is protective in neurons, making BI-1 an interesting target for future studies aiming at the inhibition of neuronal cell death during neurodegenerative diseases and stroke.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins
  • Cell Death / drug effects
  • Cell Line
  • Endoplasmic Reticulum / metabolism
  • Enzyme Inhibitors / pharmacology
  • Glucose / metabolism*
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Neuroprotective Agents / metabolism*
  • Oxygen / metabolism*
  • Rats
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / metabolism
  • Thapsigargin / pharmacology


  • Apoptosis Regulatory Proteins
  • Enzyme Inhibitors
  • Membrane Proteins
  • Neuroprotective Agents
  • Recombinant Fusion Proteins
  • Tmbim6 protein, rat
  • Thapsigargin
  • Glucose
  • Oxygen