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[PMID]: 29298868
[Au] Autor:Marks KL; Martel DT; Wu C; Basura GJ; Roberts LE; Schvartz-Leyzac KC; Shore SE
[Ad] Address:Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, MI 48109, USA.
[Ti] Title:Auditory-somatosensory bimodal stimulation desynchronizes brain circuitry to reduce tinnitus in guinea pigs and humans.
[So] Source:Sci Transl Med;10(422), 2018 Jan 03.
[Is] ISSN:1946-6242
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The dorsal cochlear nucleus is the first site of multisensory convergence in mammalian auditory pathways. Principal output neurons, the fusiform cells, integrate auditory nerve inputs from the cochlea with somatosensory inputs from the head and neck. In previous work, we developed a guinea pig model of tinnitus induced by noise exposure and showed that the fusiform cells in these animals exhibited increased spontaneous activity and cross-unit synchrony, which are physiological correlates of tinnitus. We delivered repeated bimodal auditory-somatosensory stimulation to the dorsal cochlear nucleus of guinea pigs with tinnitus, choosing a stimulus interval known to induce long-term depression (LTD). Twenty minutes per day of LTD-inducing bimodal (but not unimodal) stimulation reduced physiological and behavioral evidence of tinnitus in the guinea pigs after 25 days. Next, we applied the same bimodal treatment to 20 human subjects with tinnitus using a double-blinded, sham-controlled, crossover study. Twenty-eight days of LTD-inducing bimodal stimulation reduced tinnitus loudness and intrusiveness. Unimodal auditory stimulation did not deliver either benefit. Bimodal auditory-somatosensory stimulation that induces LTD in the dorsal cochlear nucleus may hold promise for suppressing chronic tinnitus, which reduces quality of life for millions of tinnitus sufferers worldwide.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  2 / 22390 MEDLINE  
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[PMID]: 29293291
[Au] Autor:Ishikawa A; Ohtsuki S; Yamada S; Uwabe C; Imai H; Matsuda T; Takakuwa T
[Ad] Address:Human Health Science, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.
[Ti] Title:Formation of the Periotic Space During the Early Fetal Period in Humans.
[So] Source:Anat Rec (Hoboken);301(4):563-570, 2018 Apr.
[Is] ISSN:1932-8494
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The inner ear is a very complicated structure, composed of a bony labyrinth (otic capsule; OC), membranous labyrinth, with a space between them, named the periotic labyrinth or periotic space. We investigated how periotic tissue fluid spaces covered the membranous labyrinth three-dimensionally, leading to formation of the periotic labyrinth encapsulated in the OC during human fetal development. Digital data sets from magnetic resonance images and phase-contrast X-ray tomography images of 24 inner ear organs from 24 human fetuses from the Kyoto Collection (fetuses in trimesters 1 and 2; crown-rump length: 14.4-197 mm) were analyzed. The membranous labyrinth was morphologically differentiated in samples at the end of the embryonic period (Carnegie stage 23), and had grown linearly to more than eight times in size during the observation period. The periotic space was first detected at the 35-mm samples, around the vestibule and basal turn of the cochlea, which elongated rapidly to the tip of the cochlea and semicircular ducts, successively, and almost covered the membranous labyrinth at the 115-mm CRL stage or later. In those samples, several ossification centers were detected around the space. This article thus demonstrated that formation of the membranous labyrinth, periotic space (labyrinth), and ossification of the OC occurs successively, according to an intricate timetable. Anat Rec, 301:563-570, 2018. © 2018 Wiley Periodicals, Inc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1002/ar.23764

  3 / 22390 MEDLINE  
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[PMID]: 29439202
[Au] Autor:Moglie MJ; Fuchs PA; Elgoyhen AB; Goutman JD
[Ad] Address:Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres," Consejo Nacional de Investigaciones Científicas y Técnicas (INGEBI-CONICET), 1428 Buenos Aires, Argentina.
[Ti] Title:Compartmentalization of antagonistic Ca signals in developing cochlear hair cells.
[So] Source:Proc Natl Acad Sci U S A;115(9):E2095-E2104, 2018 Feb 27.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:During a critical developmental period, cochlear inner hair cells (IHCs) exhibit sensory-independent activity, featuring action potentials in which Ca ions play a fundamental role in driving both spiking and glutamate release onto synapses with afferent auditory neurons. This spontaneous activity is controlled by a cholinergic input to the IHC, activating a specialized nicotinic receptor with high Ca permeability, and coupled to the activation of hyperpolarizing SK channels. The mechanisms underlying distinct excitatory and inhibitory Ca roles within a small, compact IHC are unknown. Making use of Ca imaging, afferent auditory bouton recordings, and electron microscopy, the present work shows that unusually high intracellular Ca buffering and "subsynaptic" cisterns provide efficient compartmentalization and tight control of cholinergic Ca signals. Thus, synaptic efferent Ca spillover and cross-talk are prevented, and the cholinergic input preserves its inhibitory signature to ensure normal development of the auditory system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1719077115

  4 / 22390 MEDLINE  
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[PMID]: 29436610
[Au] Autor:Song YL; Tian KY; Mi WJ; Ding ZJ; Qiu Y; Chen FQ; Zha DJ; Qiu JH
[Ad] Address:Department of Otolaryngology­Head and Neck Surgery, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
[Ti] Title:Decreased expression of TERT correlated with postnatal cochlear development and proliferation reduction of cochlear progenitor cells.
[So] Source:Mol Med Rep;17(4):6077-6083, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Cochlear progenitor cells are considered as one of the best candidates for hair cell regeneration, thus, the regulation of cochlear progenitor cell proliferation has become a focus in this field. Several genes expressed in the inner ear during postnatal development have been demonstrated to be involved in maintaining the proliferative potential of progenitor cells, but the mechanism for regulating the proliferation and differentiation of cochlear progenitor cells remains poorly understood. Telomerase reverse transcriptase (TERT) has rate limiting telomerase activity and the overexpression of TERT has been shown to promote cell proliferation in series of cell lines. The aim of the present study was to evaluate the expression of TERT in the postnatal development of the cochlea and progenitor cells. The results demonstrated that TERT was expressed in the basilar membranes during the first postnatal week. In vitro, TERT expression in progenitor cells reached a maximum at day 4 after culture and decreased as the culture time prolonged or the cell passage number increased. These results led us to hypothesize that TERT may be involved in the development of the cochlea and in maintaining the proliferation ability of progenitor cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8565

  5 / 22390 MEDLINE  
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[PMID]: 29429820
[Au] Autor:Rigato C; Reinfeldt S; Håkansson B; Fredén Jansson KJ; Renvall E; Eeg-Olofsson M
[Ad] Address:Division of Signal Processing and Biomedical Engineering, Department of Electrical Engineering, Chalmers University of Technology, SE-412 96 Gothenburg, Sweden. Electronic address: rigato@chalmers.se.
[Ti] Title:Direct bone conduction stimulation: Ipsilateral effect of different transducer attachments in active transcutaneous devices.
[So] Source:Hear Res;361:103-112, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Active transcutaneous bone conduction devices, where the transducer is implanted, are used for rehabilitation of hearing impaired patients by directly stimulating the skull bone. The transducer and the way it is attached to the bone play a central role in the design of such devices. The actual effect of varying the contact to bone has not been addressed yet. The aim of this study is therefore to compare how different attachment methods of the transducer to the bone for direct stimulation affect the ear canal sound pressure and vibration transmission to the ipsilateral cochlea. Three different attachments to the bone were tested: (A) via a flat small-sized surface, (B) via a flat wide surface and (C) via two separated screws. Measurements were done on four human heads on both sides. The attachments were compared in terms of induced cochlear promontory velocity, measured by a laser Doppler vibrometer, and ear canal sound pressure, measured by a low noise microphone. A swept sine stimulus was used in the frequency range 0.1-10 kHz. On an average level, the attachment method seems to affect the transmission mainly at frequencies above 5 kHz. Furthermore, the results suggest that a smaller contact surface might perform better in terms of transmission of vibrations at mid and high frequencies. However, when considering the whole frequency range, average results from the different attachment techniques are comparable.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  6 / 22390 MEDLINE  
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[PMID]: 29426600
[Au] Autor:Ohlemiller KK; Kaur T; Warchol ME; Withnell RH
[Ad] Address:Washington University School of Medicine, Department of Otolaryngology, Central Institute for the Deaf at Washington University School of Medicine, Fay and Carl Simons Center for Hearing and Deafness, Saint Louis MO, USA. Electronic address: kohlemiller@wustl.edu.
[Ti] Title:The endocochlear potential as an indicator of reticular lamina integrity after noise exposure in mice.
[So] Source:Hear Res;361:138-151, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The endocochlear potential (EP) provides part of the electrochemical drive for sound-driven currents through cochlear hair cells. Intense noise exposure (110 dB SPL, 2 h) differentially affects the EP in three inbred mouse strains (C57BL/6 [B6], CBA/J [CBA], BALB/cJ [BALB]) (Ohlemiller and Gagnon, 2007, Hearing Research 224:34-50; Ohlemiller et al., 2011, JARO 12:45-58). At least for mice older than 3 mos, B6 mice are unaffected, CBA mice show temporary EP reduction, and BALB mice may show temporary or permanent EP reduction. EP reduction was well correlated with histological metrics for injury to stria vascularis and spiral ligament, and little evidence was found for holes or tears in the reticular lamina that might 'short out' the EP. Thus we suggested that the genes and processes that underlie the strain EP differences primarily impact cochlear lateral wall, not the organ of Corti. Our previous work did not test the range of noise exposure conditions over which strain differences apply. It therefore remained possible that the relation between exposure severity and acute EP reduction simply has a higher exposure threshold in B6 mice compared to CBA and BALB. We also did not test for age dependence. It is well established that young adult animals are especially vulnerable to noise-induced permanent threshold shifts (NIPTS). It is unknown, however, whether heightened vulnerability of the lateral wall contributes to this condition. The present study extends our previous work to multiple noise exposure levels and durations, and explicitly compares young adult (6-7 wks) and older mice (>4 mos). We find that the exposure level-versus-acute EP relation is dramatically strain-dependent, such that B6 mice widely diverge from both CBA and BALB. For all three strains, however, acute EP reduction is greater in young mice. Above 110 dB SPL, all mice exhibited rapid and severe EP reduction that is likely related to tearing of the reticular lamina. By contrast, EP-versus-noise duration examined at 104 dB suggested that different processes contribute to EP reduction in young and older mice. The average EP falls to a constant level after ∼7.5 min in older mice, but progressively decreases with further exposure in young mice. Confocal microscopy of organ of Corti surface preparations stained for phalloidin and zonula occludens-1 (ZO-1) indicated this corresponds to rapid loss of outer hair cells (OHCs) and formation of both holes and tears in the reticular lamina of young mice. In addition, when animals exposed at 119 dB were allowed to recover for 1 mo, only young B6 mice showed collapse of the EP to ≤5 mV. Confocal analysis suggested novel persistent loss of tight junctions in the lateral organ of Corti. This may allow paracellular leakage that permanently reduces the EP. From our other findings, we propose that noise-related lateral wall pathology in young CBA and BALB mice promotes hair cell loss and opening of the reticular lamina. The heightened vulnerability of young adult animals to noise exposure may in part reflect special sensitivity of the organ of Corti to acute lateral wall dysfunction at younger ages. This feature appears genetically modifiable.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  7 / 22390 MEDLINE  
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[PMID]: 29395614
[Au] Autor:Jiang L; Xu J; Jin R; Bai H; Zhang M; Yang S; Zhang X; Zhang X; Han Z; Zeng S
[Ad] Address:Beijing Key Laboratory of Gene Resource and Molecular Development, Beijing Normal University, 100875, China.
[Ti] Title:Transcriptomic analysis of chicken cochleae after gentamicin damage and the involvement of four signaling pathways (Notch, FGF, Wnt and BMP) in hair cell regeneration.
[So] Source:Hear Res;361:66-79, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Unlike mammalian hair cells, which are essentially unable to regenerate after damage, avian hair cells have a robust capacity for regeneration. The prerequisite for understanding the above difference is knowing the genetic programming of avian hair cell regeneration. Although the major processes have been known, the precise molecular signaling that induces regeneration remains unclear. To address this issue, we performed a high-throughput transcriptomic analysis of gene expression during hair cell regeneration in the chick cochlea after antibiotic injury in vivo. A total of 16,588 genes were found to be expressed in the cochlea, of which about 1000 genes were differentially expressed among the four groups studied, i.e., 2 days (d) or 3 d post-treatment with gentamicin or physiological saline. The differentially expressed genes were distributed across approximately one hundred signaling pathways, including the Notch, MAPK (FGF), Wnt and TGF-ß (BMP) pathways that have been shown to play important roles in embryonic development. Some differentially expressed genes (2-3 in each pathway) were further verified by qRT-PCR. After blocking Notch, FGF or BMP signaling, the number of regenerating hair cells and mitotic supporting cells increased. However, the opposite effect was observed after suppressing the Wnt pathway or enhancing BMP signaling. To our knowledge, the present study provided a relatively complete dataset of candidate genes and signaling pathways most likely involved in hair cell regeneration and should be a useful start in deciphering the genetic circuitry for inducing hair cell regeneration in the chick cochlea.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  8 / 22390 MEDLINE  
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[PMID]: 29352609
[Au] Autor:Setz C; Benischke AS; Pinho Ferreira Bento AC; Brand Y; Levano S; Paech F; Leitmeyer K; Bodmer D
[Ad] Address:Department of Biomedicine, University of Basel, Hebelstrasse 20, 4031, Basel, Switzerland; Clinic for Otolaryngology, Head and Neck Surgery, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland.
[Ti] Title:Induction of mitophagy in the HEI-OC1 auditory cell line and activation of the Atg12/LC3 pathway in the organ of Corti.
[So] Source:Hear Res;361:52-65, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Autophagy is a highly evolutionary conserved quality control defense mechanism within cells, which has also been implicated in cell death processes. In the mammalian inner ear, autophagy has been shown to play a role during early morphogenesis as well as in adult cochlear hair cells exposed to ototoxic insults. Mitophagy, a selective autophagic cell process targeting mitochondria, hasn't been studied in the inner ear so far. On this work, we searched for molecular indicators of mitophagy within House Ear Institute-Organ of Corti-1 (HEI-OC1) cells as well as in the organ of Corti (OC). We first tested for the expression of Pink1/Park2 mRNA in 5-day-old C57BL/6 mice's cochleae using RT-PCR. We focused on the induction of mitophagy in HEI-OC1 cells as well as in the OC and investigated a possible mitophagic potential of the aminoglycoside agent gentamicin. The induction of mitophagy in HEI-OC1 cells was detected by objectivizing the translocation of fluorescence-tagged LC3 to mitochondria using confocal microscopy after a 6-h incubation with a well-described mitochondrial uncoupler and mitophagy-inducing agent: carbonyl cyanide m-chlorophenyl hydrazone (CCCP). Incubation with gentamicin generated no mitochondrial translocation of LC3. Protein levels of COXIV, Atg5/12 and LC3 were evaluated by an immunoblot analysis after a 24-h CCCP treatment as well as gentamicin. We demonstrated mitophagy after CCCP exposure in HEI-OC1 cells by showing a downregulation of COXIV. A downregulation of COXIV could also be visualized in the OC after CCCP. A significant oxygen consumption rate (OCR) changed in cells treated with CCCP as well as significant morphological changes of mitochondria by electron microscopy (EM) strengthen this assumption. Gentamicin exposure generated no impact on OCR or mitochondrial morphological changes by EM. Finally, we demonstrated changes in the expression of Atg12 and LC3 proteins in both the OC and HEI-OC1 cells after CCCP exposure but not after gentamicin. Our data indicate that gentamicin had no impact in the activation of mitophagy-neither in the HEI-OC1 cell line nor in the OC. Therefore, we speculate that mitophagic-independent mechanisms may underly aminoglycoside ototoxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  9 / 22390 MEDLINE  
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[PMID]: 29429180
[Au] Autor:Hu J; Chen ZC; Zhang YZ; Han P; Ma WJ; Zhang Q; Xu M
[Ad] Address:Department of Otorhinolaryngology Head and Neck Surgery, Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an 710004, China.
[Ti] Title:[The experimental study on endoplasmic reticulum stress-participated outer hair cell apoptosis in cadherin 23 gene mutant mice].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(2):110-117, 2018 Feb 07.
[Is] ISSN:1673-0860
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:To test the mechanism and upstream pathway of outer hair cell apoptosis in Cadherin 23 (Cdh23) gene mutant mice. The mutant 23 ( ) 57 /6 ( 6) . 70 . - ( ) . ( ) ( ) . - - ( ) / ( ) . . . 23 . The ABR thresholds in mice were significantly higher than those in B6 mice at the age of 1 and 3 months (both <0.05). The surface preparation with TUNEL staining confirmed OHC apoptosis in mouse cochleae which showed a higher TUNEL positive cell ratio than B6 mouse( =11.291, <0.01). The ER stress marker and mRNA were upregulated in the mouse inner ear, when compared with those in the B6 mouse(both <0.05). The BiP protein extracted from the mouse cochleae was significantly higher than that of B6 mouse measured by Western blot ( =3.66, =0.02). Immunostaining showed that BiP and CHOP were highly detected in the OHC in mouse cochleae, and was mainly detected in the perinuclear region of OHC. However, a bare BiP and CHOP signal were shown in B6 mouse cochleae. The CDH23 protein was specifically localized at the top of the OHC in B6 mice, indicating the localization of the tip links in hair bundle stereocilia. On the contrary, the CDH23 protein was found to be localized from the top to the nuclei of the OHC in mice. Portions of the CDH23 proteins failed to reach the top of the hair bundles and remained in the OHC cytoplasm. As the downstream response of the Cdh23 gene mutation, portions of the mutant CDH23 protein was accumulated in ER lumen resulting in the increase of ER loading and ultimately triggered ER stress and hair cell apoptosis in mouse cochleae.
[Mh] MeSH terms primary: Apoptosis/genetics
Cadherins/genetics
Endoplasmic Reticulum Stress/genetics
Hair Cells, Auditory, Outer/pathology
[Mh] MeSH terms secundary: Animals
Blotting, Western
Cochlea/pathology
Endoplasmic Reticulum Stress/physiology
Evoked Potentials, Auditory, Brain Stem
Hair Cells, Vestibular
In Situ Nick-End Labeling
Lymphokines/metabolism
Mice
Mice, Inbred C57BL
Mutation
RNA, Messenger/metabolism
Reverse Transcriptase Polymerase Chain Reaction
Transcription Factor CHOP/genetics
Transcription Factor CHOP/metabolism
Up-Regulation
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Cadherins); 0 (Cdh23 protein, mouse); 0 (Lymphokines); 0 (RNA, Messenger); 0 (immunoglobulin-binding factors); 147336-12-7 (Transcription Factor CHOP)
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.02.006

  10 / 22390 MEDLINE  
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[PMID]: 29429181
[Au] Autor:Chen T; Zhang W; Liang Y; Li Q; Yang C; Yuan YX; Ban ML
[Ad] Address:Department of Otorhinolaryngology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
[Ti] Title:[Effect of melatonin on expression of Prestin protein in the inner ear of mice following radiotherapy].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(2):118-123, 2018 Feb 07.
[Is] ISSN:1673-0860
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:To investigate the effect of melatonin on the expression of prestin protein in the inner ear of mice following a single dose radiation therapy, so as to provide the basis for the mechanism study of radiation induced inner ear injury and its prevention. Sixty 4-week-old male mice were randomly divided into six groups, including the control group (A group), 50 mg/kg MLT group (B group), 5 mg/kg MLT group (C group), 50 mg/kg MLT + radiotherapy group (D group), 5 mg/kg MLT+ radiotherapy group (E group), and 16 Gy radiotherapy group (F group). Each experimental group was randomly subdivided into two subgroups, which were killed to harvest the cochlea on the 3rd and 7th days following 16 Gy radiation. The specimens were used for immunostaining and Western blot to detect the expression of prestin protein. SPSS 19.0 software was used for statistical analysis. Prestin protein mainly distributed in the lateral membrane above the outer hair cell nucleus. When compared with A, B and C group, the expression of prestin protein in the inner ear was significantly up-regulated in F group ( <0.05). However, D and E group reduced the abnormal expression of prestin following radiotherapy when compared with F group, the difference was statistically significant ( <0.05), and the effect of D group was more significant than E group ( <0.05). The prestin protein of cochlea is mainly distributed in the lateral membrane above the outer hair cell nucleus. Following the high-dose radiotherapy, the prestin expression is upregulated, and melatonin can control the abnormal expression of prestin protein induced by radiotherapy with dose dependent.
[Mh] MeSH terms primary: Ear, Inner/metabolism
Ear, Inner/radiation effects
Hair Cells, Auditory, Outer/metabolism
Melatonin/pharmacology
Molecular Motor Proteins/metabolism
[Mh] MeSH terms secundary: Animals
Cochlea/drug effects
Cochlea/radiation effects
Hair Cells, Auditory, Outer/drug effects
Hair Cells, Auditory, Outer/radiation effects
Male
Mice
Random Allocation
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Molecular Motor Proteins); 0 (Pres protein, mouse); JL5DK93RCL (Melatonin)
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.02.007


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