Transient protection by peripheral benzodiazepine receptors during the early events of ultraviolet light-induced apoptosis

Cell Death Differ. 2001 Jul;8(7):747-53. doi: 10.1038/sj.cdd.4400861.

Abstract

The peripheral benzodiazepine receptor (PBR) is a mitochondrial protein involved in the formation of mitochondrial permeability transition (PT) pores which play a critical role during the early events of apoptosis. PBRs are located in many tissues and are strongly expressed in the superficial layers of human epidermis. PBRs play a protective role against free radical damage and PBR ligands modulate apoptosis. To investigate the role of PBR during the early events of ultraviolet (UV)-mediated apoptosis we compared the effects of UVB on PBR-transfected Jurkat cells and their wild type counterparts devoid of any PBR expression. Results indicate that early after UVB exposure (up to 4 h), PBR-transfected cells were more resistant to apoptosis and exhibited a delayed mitochondrial transmembrane potential drop, a diminished superoxide anions production, and a reduced caspase-3 activation. Taken together these findings suggest that PBR may regulate early death signals leading to UV induced apoptosis.

MeSH terms

  • Apoptosis / radiation effects*
  • Caspase 3
  • Caspases / metabolism
  • Enzyme Activation / radiation effects
  • Humans
  • Intracellular Membranes / metabolism
  • Intracellular Membranes / radiation effects
  • Jurkat Cells
  • Membrane Potentials / radiation effects
  • Mitochondria / metabolism
  • Mitochondria / radiation effects
  • Permeability / radiation effects
  • Receptors, GABA-A / genetics
  • Receptors, GABA-A / metabolism*
  • Superoxides / metabolism
  • Transfection
  • Ultraviolet Rays*

Substances

  • Receptors, GABA-A
  • Superoxides
  • CASP3 protein, human
  • Caspase 3
  • Caspases