UCP2 protects hypothalamic cells from TNF-alpha-induced damage

FEBS Lett. 2008 Sep 3;582(20):3103-10. doi: 10.1016/j.febslet.2008.08.006. Epub 2008 Aug 12.

Abstract

Uncoupling protein 2 (UCP2) is highly expressed in the hypothalamus; however, little is known about the functions it exerts in this part of the brain. Here, we hypothesized that UCP2 protects hypothalamic cells from oxidative and pro-apoptotic damage generated by inflammatory stimuli. Intracerebroventricular injection of tumor necrosis factor alpha (TNF-alpha)-induced an increase of UCP2 expression in the hypothalamus, which was accompanied by increased expression of markers of oxidative stress and pro-apoptotic proteins. The inhibition of UCP2 expression by an antisense oligonucleotide enhanced the damaging effects of TNF-alpha. Conversely, increasing the hypothalamic expression of UCP2 by cold exposure reversed most of the effects of the cytokine. Thus, UCP2 acts as a protective factor against cellular damage induced by an inflammatory stimulus in the hypothalamus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cells, Cultured
  • Cold Temperature
  • Hypothalamus / cytology*
  • Hypothalamus / metabolism*
  • Ion Channels / antagonists & inhibitors
  • Ion Channels / biosynthesis
  • Ion Channels / physiology*
  • Male
  • Mitochondrial Proteins / antagonists & inhibitors
  • Mitochondrial Proteins / biosynthesis
  • Mitochondrial Proteins / physiology*
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / pharmacology
  • Tumor Necrosis Factor-alpha / physiology
  • Uncoupling Protein 2

Substances

  • Ion Channels
  • Mitochondrial Proteins
  • Tumor Necrosis Factor-alpha
  • Ucp2 protein, rat
  • Uncoupling Protein 2