G protein-associated, specific membrane binding sites mediate the neuroprotective effect of dehydroepiandrosterone

FASEB J. 2006 Mar;20(3):577-9. doi: 10.1096/fj.05-5078fje. Epub 2006 Jan 11.

Abstract

The neurosteroid dehydroepiandrosterone (DHEA) at 1 nM protects NMDA-/GABAA-receptor negative neural crest-derived PC12 cells from apoptosis. We now report that membrane-impermeable DHEA-BSA conjugate replaces unconjugated DHEA in protecting serum-deprived PC12 cells from apoptosis (IC50=1.5 nM). Protection involves phosphorylation of the prosurvival factor Src and induction of the anti-apoptotic protein Bcl-2 and is sensitive to pertussis toxin. Binding assays of [3H]DHEA on isolated PC12 cell membranes revealed saturation within 30 min and binding of DHEA with a Kd of 0.9 nM. A similar binding activity was detectable in isolated membranes from rat hippocampus and from normal human adrenal chromaffin cells. The presence of DHEA-specific membrane binding sites was confirmed by flow cytometry and confocal laser microscopy of DHEA-BSA-FITC stained cells. In contrast to estrogens and progestins, glucocorticoids and androgens displaced DHEA from its membrane binding sites but with a 10-fold lower affinity than DHEA (IC50=9.3 and 13.6 nM, respectively). These agents acted as pure antagonists, blocking the antiapoptotic effect of DHEA as well as the induction of Bcl-2 proteins and Src kinase activation. In conclusion, our findings suggest that neural crest-derived cells possess specific DHEA membrane binding sites coupled to G proteins. Binding to these sites confers neuroprotection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenal Medulla / cytology
  • Androgens / pharmacology
  • Animals
  • Apoptosis / drug effects
  • Cell Membrane / drug effects
  • Chromaffin Cells / drug effects
  • Chromaffin Cells / metabolism
  • Culture Media, Serum-Free / pharmacology
  • Dehydroepiandrosterone / analogs & derivatives
  • Dehydroepiandrosterone / metabolism
  • Dehydroepiandrosterone / pharmacology*
  • Estrogens / pharmacology
  • Glucocorticoids / pharmacology
  • Guanosine 5'-O-(3-Thiotriphosphate) / metabolism
  • Hippocampus / cytology
  • Hippocampus / drug effects
  • Humans
  • Male
  • Microscopy, Confocal
  • Neuroprotective Agents / metabolism
  • Neuroprotective Agents / pharmacology*
  • PC12 Cells / drug effects
  • Pertussis Toxin / pharmacology
  • Proto-Oncogene Proteins c-bcl-2 / physiology
  • Rats
  • Receptors, G-Protein-Coupled / drug effects*
  • Receptors, G-Protein-Coupled / metabolism
  • Receptors, GABA-A / physiology
  • Receptors, N-Methyl-D-Aspartate / physiology
  • Receptors, Steroid / drug effects*
  • Receptors, Steroid / metabolism
  • Serum Albumin, Bovine / pharmacology
  • bcl-X Protein / physiology

Substances

  • Androgens
  • Culture Media, Serum-Free
  • Estrogens
  • Glucocorticoids
  • Neuroprotective Agents
  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, G-Protein-Coupled
  • Receptors, GABA-A
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Steroid
  • bcl-X Protein
  • dehydroepiandrosterone receptor
  • dehydroepiandrosterone-bovine serum albumin
  • Serum Albumin, Bovine
  • Guanosine 5'-O-(3-Thiotriphosphate)
  • Dehydroepiandrosterone
  • Pertussis Toxin