Document Detail


Characterization of neuronal cell death in the spiral ganglia of a mouse model of endolymphatic hydrops.
MedLine Citation:
PMID:  23462289     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
HYPOTHESIS: Spiral ganglion neurons (SGN) in the Phex male mouse, a murine model of postnatal endolymphatic hydrops (ELH) undergo progressive deterioration reminiscent of human and other animal models of ELH with features suggesting apoptosis as an important mechanism.
BACKGROUND: Histologic analysis of the mutant's cochlea demonstrates ELH by postnatal Day (P) 21 and SGN loss by P90. The SGN loss seems to occur in a consistent topographic pattern beginning at the cochlear apex.
METHODS: SGN were counted at P60, P90, and P120. Semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR), quantitative PCR, and immunohistochemical analyses of activated caspase-3, caspase-8, and caspase-9 were performed on cochlear sections obtained from mutants and controls. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling assay (TUNEL) was carried out on 2 mutants and 2 controls.
RESULTS: Corrected SGN counts in control mice were greater in the apical turn of the cochleae at P90 and P120, respectively (p < 0.01). Increased expression of activated caspase-3, caspase-8, and caspase-9 was seen in the mutant. At later time points, activated caspase expression gradually declined in the apical turns and increased in basal turns of the cochlea. Quantitative and semiquantitative PCR analysis confirmed increased expression of caspase-3, caspase-8, and caspase-9 at P21 and P40. TUNEL staining demonstrated apoptosis at P90 in the apical and basal turns of the mutant cochleae.
CONCLUSION: SGN degeneration in the Phex /Y mouse seems to mimic patterns observed in other animals with ELH. Apoptosis plays an important role in the degeneration of the SGN in the Phex male mouse.
Authors:
Maroun T Semaan; Qing Y Zheng; Fengchan Han; Yuxi Zheng; Heping Yu; John C Heaphy; Cliff A Megerian
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology     Volume:  34     ISSN:  1537-4505     ISO Abbreviation:  Otol. Neurotol.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-03-15     Completed Date:  2013-09-13     Revised Date:  2014-04-02    
Medline Journal Info:
Nlm Unique ID:  100961504     Medline TA:  Otol Neurotol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  559-69     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Caspase 3 / metabolism
Caspase 8 / metabolism
Caspase 9 / metabolism
Disease Models, Animal
Disease Progression
Endolymphatic Hydrops / metabolism,  pathology*
Male
Mice
Neurons / metabolism,  pathology*
Spiral Ganglion / metabolism,  pathology*
Grant Support
ID/Acronym/Agency:
R01 DC007392/DC/NIDCD NIH HHS; R01 DC009246/DC/NIDCD NIH HHS; R01DC007392/DC/NIDCD NIH HHS; R01DC009246/DC/NIDCD NIH HHS
Chemical
Reg. No./Substance:
EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspase 9
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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