Gene expression profiling of DBA/2J mice cochleae treated with l-methionine and valproic acid
Author(s) -
Fuyuki Miya,
Hideki Mutai,
Masato Fujii,
Keith A. Boroevich,
Tatsuo Matsunaga,
Tatsuhiko Tsunoda
Publication year - 2015
Publication title -
genomics data
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.549
H-Index - 20
ISSN - 2213-5960
DOI - 10.1016/j.gdata.2015.06.022
Subject(s) - hearing loss , epigenetics , valproic acid , gene expression profiling , histone , methionine , auditory brainstem response , cochlea , gene , biology , gene expression , cancer research , medicine , bioinformatics , genetics , epilepsy , neuroscience , audiology , amino acid
DBA/2J mice, which have homozygous mutations in Cdh23 and Fscn2, are characterized by early onset hearing loss at as early as three-weeks of age (Noben-Trauth et al., 2003 [1]) and are an animal model for progressive hearing loss research. Recently, it has been reported that epigenetic regulatory pathways likely play an important role in hearing loss (Provenzano and Domann, 2007 [2]; Mutai et al., 2009 [3]; Waldhaus et al., 2012 [4]). We previously reported that DBA/2J mice injected subcutaneously with a combination of epigenetic modifying reagents, l-methionine (MET) as methyl donor and valproic acid (VPA) as a pan-histone deacetylases (Hdac) inhibitor, showed a significant attenuation of progressive hearing loss by measuring their auditory brainstem response (ABR) thresholds (Mutai et al., 2015 [5]). Here we present genome wide expression profiling of the DBA/2J mice cochleae, with and without treatment of MET and VPA, to identify the genes involved in the reduction of progressive hearing loss. The raw and normalized data were deposited in NCBI's Gene Expression Omnibus (GEO ID: GSE62173) for ease of reproducibility and reanalysis.
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