A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift

Int J Audiol. 2016 Oct;55(10):571-9. doi: 10.1080/14992027.2016.1192693. Epub 2016 Jul 11.

Abstract

Objective: A non-synonymous single nucleotide polymorphism (rs61742642; C to T, P386S) in the ligand-binding domain of human estrogen-related receptor beta (ESRRβ) showed possible association to noise-induced hearing loss (NIHL) in our previous study.

Design: This study was conducted to examine the effect of the ESRRβ rs61742642 T variant on temporary threshold shift (TTS). TTS was induced by 10 minutes of exposure to audiometric narrow-band noise centered at 2000 Hz. Hearing thresholds and distortion product otoacoustic emissions input output function (DP IO) at 2000, 3000, and 4000 Hz were measured before and after the noise exposure.

Study sample: Nineteen participants with rs61742642 CT genotype and 40 participants with rs61742642 CC genotype were recruited for the study.

Results: Participants with the CT genotype acquired a significantly greater TTS without convincing evidence of greater DP IO temporary level shift (DPTLS) compared to participants with the CC genotype.

Conclusion: The results indicated that the ESRRβ polymorphism is associated with TTS. Future studies were recommended to explore molecular pathways leading to increased susceptibility to NIHL.

Keywords: Estrogen-Related Receptor Beta (ESRRβ); Noise-induced hearing loss (NIHL); Otoacoustic Emissions (OAE); Single Nucleotide Polymorphism (SNP); Temporary Threshold Shift (TTS).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acoustic Stimulation
  • Audiometry, Pure-Tone
  • Auditory Fatigue*
  • Case-Control Studies
  • Female
  • Genetic Association Studies
  • Genetic Predisposition to Disease
  • Hearing Loss, Noise-Induced / diagnosis
  • Hearing Loss, Noise-Induced / genetics*
  • Hearing Loss, Noise-Induced / physiopathology
  • Heterozygote
  • Homozygote
  • Humans
  • Male
  • Otoacoustic Emissions, Spontaneous
  • Phenotype
  • Polymorphism, Single Nucleotide*
  • Receptors, Estrogen / genetics*
  • Risk Factors

Substances

  • ESRRB protein, human
  • Receptors, Estrogen