Source:http://linkedlifedata.com/resource/pubmed/id/18355160
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2008-3-21
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| pubmed:abstractText |
Noise exposure is known to induce cell death signaling in the cochlea. Since c-Jun N-terminal kinase (JNK) signaling is known to induce both cell survival and apoptosis, the present study focused on early changes (within 24 h) after impulse noise exposure, inquiring whether cell death is always related to phosphorylation of JNK in the inner ear. Anesthetized adult albino rats were exposed to a single impulse noise exposure (194 kPa) and sacrificed 3 or 24 h later. Paraffin-embedded sections were examined for positive staining of phosphorylated JNK and the presence of cells with fragmented DNA (TUNEL staining). Positive TUNEL staining was observed at the spiral limbus and in the stria vascularis at 24 h following impulse noise exposure, but no correlation with JNK activation was found at these locations. In the hearing organ (organ of Corti) and in the lateral wall, TUNEL-reactive cells were observed at 24 h following trauma. This was preceded by p-JNK staining at 3 h, indicating JNK-activated cell death in these regions. Finally, p-JNK reactivity was observed in the spiral ganglion with no correlation to TUNEL staining within the time frame of this study. These results suggest that JNK activation following impulse noise exposure may not always be related to cell death, and conversely, some cells may die through JNK-independent signaling.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
|
| pubmed:issn |
0897-7151
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
25
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
72-7
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:18355160-Acoustic Stimulation,
pubmed-meshheading:18355160-Animals,
pubmed-meshheading:18355160-Biological Markers,
pubmed-meshheading:18355160-Cell Death,
pubmed-meshheading:18355160-Cochlea,
pubmed-meshheading:18355160-DNA Fragmentation,
pubmed-meshheading:18355160-Enzyme Activation,
pubmed-meshheading:18355160-Female,
pubmed-meshheading:18355160-Hair Cells, Auditory,
pubmed-meshheading:18355160-Hearing Loss, Noise-Induced,
pubmed-meshheading:18355160-In Situ Nick-End Labeling,
pubmed-meshheading:18355160-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:18355160-Noise,
pubmed-meshheading:18355160-Phosphorylation,
pubmed-meshheading:18355160-Rats,
pubmed-meshheading:18355160-Rats, Sprague-Dawley,
pubmed-meshheading:18355160-Signal Transduction,
pubmed-meshheading:18355160-Spiral Ganglion,
pubmed-meshheading:18355160-Time Factors
|
| pubmed:year |
2008
|
| pubmed:articleTitle |
Activation of JNK in the inner ear following impulse noise exposure.
|
| pubmed:affiliation |
Department of Otolaryngology, Kyoto-Katsura Hospital, Kyoto, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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