Transcriptional profiling of apolipoprotein-O-overexpressing H9c2 cardiomyoblasts

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.