Oxidative stress induced lipid accumulation via SREBP1c activation in HepG2 cells

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• 作者：Mika Sekiya ; Ako Hiraishi ; Maiko Touyama ; Kazuichi Sakamoto
• 关键词：Fatty acid biosynthesis ; Adipogenesis ; ROS ; Transcription factor
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2008
• 出版时间：31 October 2008
• 年：2008
• 卷：375
• 期：4
• 页码：602-607
• 全文大小：677 K

文摘

SREBP1c (sterol regulatory element-binding protein 1c) is a metabolic-syndrome-associated transcription factor that controls fatty acid biosynthesis under glucose/insulin stimulation. Oxidative stress increases lipid accumulation, which promotes the generation of reactive oxygen species (ROS). However, we know little about the role of oxidative stress in fatty acid biosynthesis. To clarify the action of oxidative stress in lipid accumulation via SREBP1c, we examined SREBP1c activity in H₂O₂-treated mammalian cells. We introduced a luciferase reporter plasmid carrying the SREBP1c-binding site into HepG2 or COS-7 cells. With increasing H₂O₂ dose, SREBP1c transcriptional activity increased in HepG2 cells but declined in COS-7 cells. RT-PCR analysis revealed that mRNA expression of SREBP1c gene or of SREBP1c-regulated genes rose H₂O₂ dose-dependently in HepG2 cells but dropped in COS-7 cells. Lipid accumulation and levels of the nuclear form of SREBP1c increased in H₂O₂-stimulated HepG2 cells. ROS may stimulate lipid accumulation in HepG2 cells via SREBP1c activation.