Brain mitochondrial uncoupling protein 2 (UCP2): a protective stress signal in neuronal injury

Biochem Pharmacol. 2002 Aug 1;64(3):363-7. doi: 10.1016/s0006-2952(02)01166-8.

Abstract

Mitochondrial uncoupling proteins (UCPs) can dissociate oxidative phosphorylation from respiration, and they appear to be critical for energy balance. One of these proteins, UCP2, is also expressed in neurons of subcortical brain regions of healthy subjects. Here, we report on the protective role of UCP2 in brain injury by revealing its early induction after lesions and its inverse relationship with activation of an apoptotic signal, caspase 3, in wild-type and UCP2 overexpressing transgenic mice.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Brain Injuries / metabolism*
  • Disease Models, Animal
  • Entorhinal Cortex / physiology
  • Entorhinal Cortex / surgery
  • Gene Transfer Techniques
  • Immunohistochemistry
  • Ion Channels
  • Learning / physiology
  • Male
  • Membrane Transport Proteins*
  • Memory / physiology
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria / metabolism*
  • Mitochondrial Proteins*
  • Nerve Degeneration
  • Neurons / metabolism*
  • Protective Agents / metabolism
  • Proteins / genetics
  • Proteins / metabolism*
  • Rats
  • Rats, Wistar
  • Signal Transduction
  • Stress, Physiological / metabolism
  • Uncoupling Protein 2

Substances

  • Ion Channels
  • Membrane Transport Proteins
  • Mitochondrial Proteins
  • Protective Agents
  • Proteins
  • Ucp2 protein, mouse
  • Ucp2 protein, rat
  • Uncoupling Protein 2