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KMID : 0361020130560050278
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Korean Journal of Otolaryngology - Head and Neck Surgery
2013 Volume.56 No. 5 p.278 ~ p.285
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Expression Changes of Endothelin-1, Endothelin Receptor A and B in the Cochlea after Noise Exposure
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Hur Gang-Min
Lyu Ah-Ra
Han Wook-Kyoung
Choi Jin-Woong
Rha Ki-Sang
Park Yong-Ho
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Abstract
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Background and Objectives: There are several evidences of reduced cochlea blood flow after noise exposure in the cochlea. However, the pathophysiology of blood flow change is still obscure, and endothelins, proteins that constrict blood vessels and play a key role in vascular homeostasis using its receptors may have importance in this respect. In this study, we investigated the expression changes of endothelin-1 (ET-1), endothelin receptor A (ETAR) and B (ETBR) according to auditory threshold change after noise exposure. Materials and Method: Mice were exposed to different noise to generate transient (group 2) and permanent threshold shift (group 3), respectively. Auditory threshold shifts were evaluated with auditory brainstem response and expression changes of ET-1, ETAR and ETBR after noise exposure were evaluated by immunohistochemistry and real time RT-PCR. Results: After noise exposure, the increased ET-1, ETAR and ETBR immunoreactivities were observe in stria vascularis, spiral ligament and spiral ganglion neuron. ET-1 mRNA expressions increased after noise exposure in both group 2 and group 3 compared to those of the control group. At 2 weeks after noise exposure, however, the ET-1 mRNA expressions in group 3 increased compared to that of the control but decreased compared to that of group 2. On the other hand, ETAR mRNA expression increased at 2 weeks after noise exposure in both groups, just after noise exposure in group 2 and at 2 weeks after noise exposure in group 3. Conclusion: These results suggest that expression changes of ET-1, ETAR and ETBR might be associated with hearing threshold shift and recovery after noise exposure in the cochlea.
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KEYWORD
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Cochlea, Endothelin receptor, Endothelin-1, Noise
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