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Transcriptional profiling of apolipoprotein-O-overexpressing H9c2 cardiomyoblasts

ABSTRACT: Mitochondrial dysfunction and excessive lipid accumulation in non-adipose tissues have been proposed widely as the roots for comorbidities generated by the growing epidemia of type 2 diabetes mellitus. Mouse models of lipotoxic cardiomyopathy have underlined this detrimental situation, but so far the proteins involved in diabetic patients’s induced mitochondrial dysfunction remain unknown. Apolipoprotein O (ApoO), originally found overexpressed in human diabetics hearts (Lamant et al. JBC 2006), is a candidate that was investigated here at the transcriptome level using H9c2 cardiomyoblasts after stable integration of an expression vector (pTT-ApoO) constitutively expressing ApoO.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE34076 | GEO | 2014/12/30

SECONDARY ACCESSION(S): PRJNA150003

REPOSITORIES: GEO

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