Molecular Mediators of Estrogen Reduction-induced Otolith Shedding

Curr Med Sci. 2021 Aug;41(4):667-672. doi: 10.1007/s11596-021-2421-3. Epub 2021 Aug 17.

Abstract

Objective: Previous study suggested that estradiol (E2) plays an important role in otolith shedding by regulating the expression of otoconin 90 (OC90). The purpose of this article is to provide further data on the effect and mechanism of E2 on the morphology of otolith.

Methods: The rats receiving bilateral ovariectomy (OVX) were used as animal models. Co-immunoprecipitation was used to observe the relationship between estrogen receptor (ER) and estrogen-related receptor α (ERRα). The morphology of otolith was observed under the scanning electron microscopy. Western blotting and qPCR were used for quantitative analysis of the roles of ER and ERRα in regulating OC90 expression.

Results: The looser otoliths were observed in rats receiving bilateral OVX, which could be reversed by supplementation with E2. The level of ERRα was decreased in bilateral OVX rats. ER and ERRα interacted with each other on the regulation of the expression of OC90.

Conclusion: Our results suggest ER and ERRα are both important downstream receptors involved in regulating OC90 expression in utricles of rats, and ERRα probably functions by interacting with ER. This provides evidence for the mechanism of otolith shedding. And it may be significant for future studies of targeted prevention and therapies for benign paroxysmal positional vertigo.

Keywords: benign paroxysmal positional vertigo; estrogen receptor; estrogen-related receptor α; otoconin 90; otolith.

MeSH terms

  • Animals
  • Calcium-Binding Proteins / genetics*
  • ERRalpha Estrogen-Related Receptor
  • Estradiol / metabolism
  • Estrogens / genetics
  • Estrogens / metabolism*
  • Female
  • Humans
  • Otolithic Membrane / metabolism*
  • Otolithic Membrane / pathology
  • Ovariectomy
  • Rats
  • Receptors, Estrogen / genetics*

Substances

  • Calcium-Binding Proteins
  • Estrogens
  • OC90 protein, human
  • Receptors, Estrogen
  • Estradiol