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ling-mei qian & xiang-qing kong month download article/chapter ling-mei qian mitochondrial death pathway xiang-qing kong fatty acid metabolism mitochondrial dna molecules related subjects congenital heart disease embryonic carcinoma cells embryonic myocardial cells caused mitochondrial dysfunction full article pdf privacy choices/manage cookies mitochondrial dna rna interference gata-4 transcription factor authors contributed equally van kempen mj fabp3 promotes apoptosis early apoptotic cells article shen cardiac myocyte apoptosis yan-hui sheng american heart association cardiac muscle tissue embryonic carcinoma european economic area induces mitochondrion impairment ventricular septal defect apoptotic/mitogenic pathways pediatr clin north flow cytometric detection fluorescein labelled annexin suppression subtractive hybridization fabp3 inhibits proliferation conditions privacy policy differentially expressed genes abnormal heart development gui-xian song yao-qiu liu hai-lang liu previous study found �low risk” neonates suitable model system check access instant access cardiac electrophysiological differentiation article journal human heart development

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         headline:Silencing of FABP3 promotes apoptosis and induces mitochondrion impairment in embryonic carcinoma cells
         description:Fatty acid binding protein 3 (FABP3) (also known as H-FABP) is a member of the intracellular lipid-binding protein family, and is mainly expressed in cardiac muscle tissue. The in vivo function of FABP3 is proposed to be in fatty acid metabolism, trafficking, and cell signaling. Our previous study found that FABP3 is highly regulated in patients with ventricular septal defect (VSD), and may play a significant role in the development of human VSD. In the present study, we aimed to investigate the impact of FABP3 knockdown by RNA interference (RNAi) on apoptosis and mitochondrial function of embryonic carcinoma (P19) cells. The results revealed that downregulated FABP3 expression promoted apoptosis, and resulted in mitochondrial deformation, increased mitochondrial membrane potential (MMP), and decreased intracellular ATP synthesis. In addition, the knockdown of FABP3 also led to excess intracellular ROS production. However, there was no obvious influence on the amount of mitochondrial DNA. Collectively, our results indicated that FABP3 knockdown promoted apoptosis and caused mitochondrial dysfunction in P19 cells, which might be responsible for the development of human VSD.
         datePublished:2012-04-20T00:00:00Z
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      headline:Silencing of FABP3 promotes apoptosis and induces mitochondrion impairment in embryonic carcinoma cells
      description:Fatty acid binding protein 3 (FABP3) (also known as H-FABP) is a member of the intracellular lipid-binding protein family, and is mainly expressed in cardiac muscle tissue. The in vivo function of FABP3 is proposed to be in fatty acid metabolism, trafficking, and cell signaling. Our previous study found that FABP3 is highly regulated in patients with ventricular septal defect (VSD), and may play a significant role in the development of human VSD. In the present study, we aimed to investigate the impact of FABP3 knockdown by RNA interference (RNAi) on apoptosis and mitochondrial function of embryonic carcinoma (P19) cells. The results revealed that downregulated FABP3 expression promoted apoptosis, and resulted in mitochondrial deformation, increased mitochondrial membrane potential (MMP), and decreased intracellular ATP synthesis. In addition, the knockdown of FABP3 also led to excess intracellular ROS production. However, there was no obvious influence on the amount of mitochondrial DNA. Collectively, our results indicated that FABP3 knockdown promoted apoptosis and caused mitochondrial dysfunction in P19 cells, which might be responsible for the development of human VSD.
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