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PARP-1-modulated AIF translocation is involved in streptomycin-induced cochlear hair cell death

Yongdong Song1,2, Zhaomin Fan1, Xiaohui Bai2,3

  • 1a Department of Otolaryngology-Head and Neck Surgery , Shangdong Provincial Hospital Affiliated to Shandong University , Jinan , PR China ;

Acta Oto-Laryngologica
|March 11, 2016
PubMed

Insights

Streptomycin (SM) causes dose-dependent hair cell death in the cochlea. Apoptosis-inducing factor (AIF) translocation, potentially modulated by PARP-1, contributes to this SM-induced ototoxicity.

Area of Science:

  • Ototoxicity research
  • Molecular mechanisms of cell death
  • Auditory neuroscience

Background:

  • Aminoglycosides like Streptomycin (SM) are common causes of sensorineural hearing loss.
  • SM-induced ototoxicity leads to sensory hair cell death.
  • The role of apoptosis-inducing factor (AIF) in SM ototoxicity requires further investigation.

Purpose of the Study:

  • To investigate the involvement of AIF in SM-induced ototoxicity.
  • To explore the potential modulation of AIF by PARP-1 in SM-treated cochlear cells.
  • To determine the dose- and location-dependency of SM-induced hair cell death.

Main Methods:

  • Cell viability assessed using MTT assay in HEI-OC1 cells.
  • Immunofluorescence used to analyze AIF, PARP-1, and myosin VIIa distribution.
  • Quantitative PCR (q-PCR) and Western-blot analyzed AIF and PARP-1 mRNA and protein expression.

Main Results:

  • SM caused dose- and location-dependent hair cell loss, worsening from apical to basal turns.
  • AIF was detected in the nucleus, with increased mRNA and altered protein distribution (decreased in mitochondria, increased in cytosol).
  • PARP-1 mRNA and protein were upregulated; the inhibitor 3-AB attenuated cell death and reversed AIF redistribution.

Conclusions:

  • SM induces dose- and location-dependent cochlear hair cell death.
  • AIF translocation from mitochondria to the nucleus/cytoplasm occurs in SM-treated hair cells.
  • PARP-1 activity appears to modulate AIF translocation and SM-induced ototoxicity.
Keywords:
HEI-OC1 cellStreptomycin ototoxicitycochleae organotypic cultureprogrammed cell death

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