Transcriptional profiling of apolipoprotein-O-overexpressing H9c2 cardiomyoblasts. Rattus norvegicus

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. Overall design: Two-condition experiment (pTT-transfected vs. pTT-ApoO-transfected H9c2 cells). Pools of transfectants are compared.

线粒体功能障碍与非脂肪组织内过量脂质蓄积，已被广泛认为是日益流行的2型糖尿病（type 2 diabetes mellitus）所引发各类并发症的核心诱因。脂毒性心肌病的小鼠模型已印证了这一有害病理状态，但目前介导糖尿病患者线粒体功能障碍的蛋白仍未明确。载脂蛋白O（Apolipoprotein O, ApoO）最初被发现于人类糖尿病心脏组织中呈高表达（Lamant 等，《Journal of Biological Chemistry》[JBC]，2006），本研究通过将组成型表达ApoO的表达载体（pTT-ApoO）稳定转染H9c2心肌成肌细胞，在转录组层面对该候选蛋白展开了相关研究。实验整体设计：设置双实验组对照（仅转染pTT空载体的H9c2细胞与转染pTT-ApoO载体的H9c2细胞），对两组转染细胞池进行比较分析。