Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens

Front Neuroendocrinol. 2009 Jul;30(2):93-105. doi: 10.1016/j.yfrne.2009.04.013. Epub 2009 May 3.

Abstract

In the present treatise, we provide evidence that the neuroprotective and mito-protective effects of estrogens are inexorably linked and involve the ability of estrogens to maintain mitochondrial function during neurotoxic stress. This is achieved by the induction of nuclear and mitochondrial gene expression, the maintenance of protein phosphatases levels in a manner that likely involves modulation of the phosphorylation state of signaling kinases and mitochondrial pro- and anti-apoptotic proteins, and the potent redox/antioxidant activity of estrogens. These estrogen actions are mediated through a combination of estrogens receptor (ER)-mediated effects on nuclear and mitochondrial transcription of protein vital to mitochondrial function, ER-mediated, non-genomic signaling and non-ER-mediated effects of estrogens on signaling and oxidative stress. Collectively, these multifaceted, coordinated action of estrogens leads to their potency in protecting neurons from a wide variety of acute insults as well as chronic neurodegenerative processes.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Calcineurin / metabolism
  • Endoplasmic Reticulum / metabolism
  • Enzyme Activation
  • Estrogens / metabolism*
  • Gene Expression Regulation
  • Humans
  • Marine Toxins
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Nerve Degeneration / metabolism
  • Neuroprotective Agents / metabolism*
  • Oxazoles / metabolism
  • Oxidation-Reduction
  • Oxidative Stress
  • Phosphoprotein Phosphatases / antagonists & inhibitors
  • Phosphoprotein Phosphatases / metabolism*
  • Signal Transduction / physiology

Substances

  • Estrogens
  • Marine Toxins
  • Neuroprotective Agents
  • Oxazoles
  • calyculin A
  • Calcineurin
  • Phosphoprotein Phosphatases