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Dysregulated gene expression in Mef2a knockout mice subjected to cardiotoxin-induced muscle injury

ABSTRACT: We identified genes expressed in mouse skeletal muscle, during the process of muscle regeneration after injury, which are dysregulated in the absence of Mef2a expression. MEF2A is a member of the evolutionarily conserved MEF2 transcription factor family which has known roles in cardiac muscle development and function, but is not well studied in skeletal muscle. We performed a comparison of gene expression profiles in wild type and MEF2A knockout tibialis anterior muscle, seven days post-injury with cardiotoxin. The results indicated that a variety of genes expressed during muscle regeneration, predominantly microRNAs in the Gtl2-Dio3 locus, are dysregulated by the loss of MEF2A expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE41871 | GEO | 2013/02/12

SECONDARY ACCESSION(S): PRJNA178361

REPOSITORIES: GEO

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Dysregulated gene expression in Mef2a knockout mice subjected to cardiotoxin-induced muscle injury

Project description:We identified genes expressed in mouse skeletal muscle, during the process of muscle regeneration after injury, which are dysregulated in the absence of Mef2a expression. MEF2A is a member of the evolutionarily conserved MEF2 transcription factor family which has known roles in cardiac muscle development and function, but is not well studied in skeletal muscle. We performed a comparison of gene expression profiles in wild type and MEF2A knockout tibialis anterior muscle, seven days post-injury with cardiotoxin. The results indicated that a variety of genes expressed during muscle regeneration, predominantly microRNAs in the Gtl2-Dio3 locus, are dysregulated by the loss of MEF2A expression. Skeletal muscle RNA used in the present study included the following two sample groups: (WT) pooled total RNA from tibialis anterior muscle taken from 5 wild type mice at seven days post-injury with 10uM cardiotoxin; (KO) pooled total RNA from tibialis anterior muscle taken from 5 Mef2a knockout mice at seven days post-injury with 10uM cardiotoxin. All mice were between 2-4 months of age. Both male and female mice were used.

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