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Sterol-regulatory-element-binding protein 1c mediates the effect of insulin on the expression of Cidea in mouse

Rui Wang1, Xingxing Kong, Anfang Cui

  • 1National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

The Biochemical Journal
|June 26, 2010
PubMed

Insights

The sterol-regulatory element-binding protein 1c (SREBP-1c) directly regulates Cidea gene expression in liver cells. Cidea then mediates SREBP-1c

Area of Science:

  • Molecular Biology
  • Metabolic Regulation
  • Gene Expression

Background:

  • The Cide (cell death-inducing DFFA-like effector) gene family is linked to lipid metabolism.
  • Cidea mRNA levels fluctuate with fasting and refeeding in mouse livers.

Purpose of the Study:

  • To investigate the molecular mechanism regulating Cidea gene expression.
  • To determine the role of SREBP-1c in mediating insulin's effect on Cidea and lipid accumulation.

Main Methods:

  • Analysis of the mouse Cidea gene promoter region to identify a sterol-regulatory element (SRE).
  • Luciferase reporter assays, electrophoretic mobility-shift assays (EMSA), and chromatin immunoprecipitation (ChIP) to confirm SREBP-1c binding.
  • Adenovirus-mediated gene manipulation (overexpression and knockdown) in mouse hepatocytes.

Main Results:

  • SREBP-1c directly binds to the identified SRE in the Cidea promoter.
  • SREBP-1c overexpression significantly increases Cidea mRNA levels.
  • Insulin and TO901317 induce Cidea expression in wild-type hepatocytes, but not in SREBP-1c-null hepatocytes.
  • Cidea overexpression promotes lipid accumulation and triglyceride storage.
  • Cidea knockdown impairs SREBP-1c-stimulated lipid accumulation.

Conclusions:

  • SREBP-1c directly mediates insulin's effect on Cidea expression in hepatocytes.
  • Cidea plays a role in SREBP-1c-dependent lipid accumulation in liver cells.

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