17β-Estradiol modulates huntingtin levels in rat tissues and in human neuroblastoma cell line

Neurosci Res. 2016 Feb:103:59-63. doi: 10.1016/j.neures.2015.07.013. Epub 2015 Aug 8.

Abstract

17β-Estradiol (E2) exerts neurotrophic and neuroprotective functions in the brain. Here, E2-induced increased levels of huntingtin (HTT), a protein involved in several crucial neuronal functions is reported. E2 physiological concentrations up-regulate HTT in hippocampus and striatum of rats as well as in human neuroblastoma cells. This effect requires both nuclear and extra-nuclear estrogen receptor (ER)α activities. Intriguingly, HTT silencing completely prevents E2 protective effects against oxidative stress injury. In conclusion, these data indicate for the first time that HTT is an E2-inducible protein involved in the first steps of E2-induced signaling pathways committed to neuronal protection against oxidative stress.

Keywords: 17-β-Estradiol; Estrogen receptor α; Human neuroblastoma cells; Huntingtin; Neuroglobin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism
  • Estradiol / metabolism*
  • Estradiol / pharmacology
  • Female
  • Gene Silencing
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Humans
  • Huntingtin Protein
  • Male
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Oxidative Stress / drug effects
  • Rats, Wistar

Substances

  • HTT protein, human
  • Htt protein, rat
  • Huntingtin Protein
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Estradiol