Abstract
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.
Highlights
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
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 panhistone deacetylases (Hdac) inhibitor, showed a significant attenuation of progressive hearing loss by measuring their auditory brainstem response (ABR) thresholds (Mutai et al, 2015 [5])
Microarray gene expression profiling to identify transcripts that are regulated by L-methionine and valproic acid in cochleae of DBA/2J mice as an animal model for hearing loss Not applicable Mice were purchased from Clea Japan (Tokyo, Japan)
Summary
The deposited data can be found at: http://www.ncbi.nlm.nih.gov/ geo/query/acc.cgi?acc=GSE62173. DBA/2J mice, which have homozygous mutations in Cdh and Fscn, are characterized by early onset hearing loss as early as three-weeks of age [1] and are an animal model for progressive hearing loss research. It has been reported that epigenetic regulatory pathways likely play an important role in hearing loss [2,3,4]. We previously reported that DBA/2J mice injected subcutaneously with a combination of epigenetic modifying reagents, l-methionine (MET) as a methyl donor and valproic acid (VPA) as a pan-histone deacetylase (Hdac) inhibitor, showed a significant attenuation of progressive hearing loss by measuring their auditory brainstem response (ABR) thresholds [5]. We investigated 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
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