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| Status |
Public on Nov 20, 2013 |
| Title |
Gene expression data from rat cochlear lateral wall after 3NP damage |
| Organism |
Rattus norvegicus |
| Experiment type |
Expression profiling by array
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| Summary |
A rat model of acute mitochondrial dysfunction in the cochlea is created by applying an irreversible mitochondrial complex II enzyme inhibitor, 3-NP, directly to the round window membrane. Treatment with 300 mM 3-NP results in temporary hearing loss (temporary threshold shift (TTS) model), whereas treatment with 500 mM 3-NP results in profound and permanent hearing loss (permanent threshold shift (PTS) model. Either treatment results with a primary histological change in the lateral wall spiral ligament. Because local ATP deprivation in the inner ear results from inhibition of inner ear mitochondrial function, this model replicates the etiology of inner ear energy failure caused by ATP deprivation due to inner ear ischemia.
We used microarrays to detail the global programme of gene expression in the damaged cochlear lateral wall by 3NP and identified distinct classes of up-regulated/ down-regulated genes during the process.
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| Overall design |
One and three day after administrated either 300 mM of 3-NP (TTS-1d and TTS-3d, respectably) or saline (Ctrl-1d and Ctrl-3d, respectably), rat cochear lateral wall in the apical side of the basal turn was harvested for RNA extraction and hybridization on Affymetrix microarrays.
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| Contributor(s) |
Tatsuo M |
| Citation missing |
Has this study been published? Please login to update or notify GEO. |
| Submission date |
Nov 19, 2013 |
| Last update date |
Mar 03, 2017 |
| Contact name |
Masato Fujioka |
| Organization name |
Keio University School of Med
|
| Department |
Otorhinolaryngology
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| Street address |
35 Shinanomachi Shinjuku
|
| City |
Tokyo |
| ZIP/Postal code |
1608582 |
| Country |
Japan |
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| Platforms (2) |
| GPL341 |
[RAE230A] Affymetrix Rat Expression 230A Array |
| GPL342 |
[RAE230B] Affymetrix Rat Expression 230B Array |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA229112 |
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