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Down-regulation of stearoyl-CoA desaturase-1 increases susceptibility to palmitic-acid-induced lipotoxicity in human trophoblast cells
Affiliation:1. Institute of Animal Molecular Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea;2. Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea;3. Department of Biomedical Sciences, Catholic Kwandong University, Gangneung, 25601, Republic of Korea;4. Center for Animal Biotechnology and Genomics and Department of Animal Science, Texas A&M University, College Station, 77843-2471, Texas, USA;1. Institute of Animal Molecular Biotechnology, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea;2. Department of Biological Sciences, Sungkyunkwan University, Suwon 16419, Republic of Korea;1. Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea;2. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon 16419, Republic of Korea
Abstract:In early pregnancy, adequate dietary factors are important for the growth of human trophoblast cells, followed by placental development. Although stearoyl-CoA desaturase 1 (SCD1) is expected to relieve palmitic acid (PA)-induced lipotoxicity by regulating diacylglycerol and ceramide, its function is unclear in human trophoblast cells. The aim was to investigate inhibitory effects of SCD1 activity on PA-induced trophoblast cell death. PA induces cell death and inhibits the invasion of human trophoblast cells (HTR8/SVneo). In addition, we demonstrate that SCD1 has a protective role against PA in human trophoblast cells by regulating AKT-mediated signaling pathway and mitochondrial membrane potential. The knockdown of SCD1 enhances the proapoptotic activity of PA in HTR8/SVneo cells. Lastly, we investigated microRNA expression predicted to target SCD1 and diacylglycerol O-acyltransferase 1 (DGAT1) by PA. Collectively, the results suggest potential roles of SCD1 and DGAT1 in alleviating the toxicity of PA and maintaining lipid homeostasis for normal placentation.
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