gms | German Medical Science

83. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

16.05. - 20.05.2012, Mainz

Molecular mechanisms of interleukin-6-induced otoprotection

Meeting Abstract

  • corresponding author Elisabeth Gerschner - Tinnituszentrums der Charité, Berlin, Germany
  • presenting/speaker Heidi Olze - Univ. HNO-Klinik, Campus Virchow, Berlin, Germany
  • presenting/speaker Agnieszka J. Szczepek - Univ. HNO-Klinik, Charité Mitte, Berlin, Germany
  • presenting/speaker Birgit Mazurek - Tinnituszentrum der Charité, Berlin, Germany

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. 83rd Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. Mainz, 16.-20.05.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12hno33

doi: 10.3205/12hno33, urn:nbn:de:0183-12hno338

Veröffentlicht: 23. Juli 2012

© 2012 Gerschner et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Integrity of the auditory sensory epithelium is the foundation for an unimpaired sequence of the process of hearing. Among the great repertoire of our modern drugs there are some, which can severely affect the hair cells’ function, such as aminoglycoside antibiotics or platinum-based chemotherapeutics. Apart from drugs, also hypoxia and noise can severely damage the auditory epithelium. Since lack of the regenerative potential in hair cells results in deafness, our aim was to identify otoprotective signalling pathways.

Based on our previous research, which demonstrated otoprotective effect of interleukin-6 (IL-6), we wanted to examine in detail the mechanism behind otoprotection induced by IL-6 and IL-6 cytokine family members.

As a research model, we used explanted organs of Corti (OC) dissected from three to five-days-old Wistar rats. The OC explants were cultured in a presence or absence of 30 ng / ml of rat recombinant IL-6. Next, using subcellular fractionation and immunoblotting, we analysed the levels of signal transducer and activator of transcription 3 (STAT-3) in the cytoplasm and in the nuclei of explants. Moreover, we determined occurrence and the level of STAT-3 phosphorylation on different residues in the cytoplasm and nuclei of the explants. In addition, we assessed the phenotype of explants by staining them with fluorescently labelled phalloidin. For a read-out, we used epifluorescence and confocal microscopy. We found that the addition of IL-6 to explant cultures induces rapid translocation of STAT-3 from cytoplasm to the nucleus. In addition, IL-6 caused phospohorylation of STAT-3 on the serine- and tyrosine- residues. Translocation coincided in time with phosophorylation.

Based on above results we hypothesize that the phosphorylation and translocation of STAT-3 could be involved in the IL6-mediated, otoprotective effect.