Silencing of FABP3 promotes apoptosis and induces mitochondrion impairment in embryonic carcinoma cells

• DOI: 10.1007/s10863-012-9439-y
• Publication Date: 2012-04-19T14:32:31Z
• Authors: Ya-Hui Shen; Gui-Xian Song; Yao-Qiu Liu; Wei Sun; Li-Juan Zhou; Hai-Lang Liu; Rong Yang; Yan-Hui Sheng; Ling-Mei Qian; Xiang-Qing Kong
• Keywords: 0301 basic medicine; Embryonal Carcinoma Stem Cells; Gene Dosage; Apoptosis; Cell Differentiation; Fatty Acid-Binding Proteins; Transfection; DNA, Mitochondrial; Mitochondria; Mice; Microscopy, Electron; 03 medical and health sciences; Adenosine Triphosphate; Gene Knockdown Techniques; Animals; RNA Interference; RNA, Messenger; Reactive Oxygen Species; Fatty Acid Binding Protein 3; Signal Transduction

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.