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Cell Type-specific Gene Expression Profiling in the Mouse Liver
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Cell Type-specific Gene Expression Profiling in the Mouse Liver

Published on: September 17, 2019

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Activation of farnesoid X receptor induces RECK expression in mouse liver

Xiaomin Peng1, Weibin Wu2, Bo Zhu1

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.

Biochemical and Biophysical Research Communications
|December 3, 2013
PubMed

Insights

Farnesoid X receptor (FXR) regulates RECK gene expression in the liver. This nuclear receptor directly binds to the RECK gene, influencing bile acid and metabolic homeostasis.

Area of Science:

  • Molecular Biology
  • Hepatology
  • Nuclear Receptor Signaling

Background:

  • Farnesoid X receptor (FXR) is a nuclear receptor crucial for regulating bile acid, lipoprotein, and glucose metabolism.
  • FXR acts as a transcription factor for various genes involved in hepatic homeostasis.

Purpose of the Study:

  • To identify novel target genes of FXR in the mouse liver.
  • To investigate the role of FXR in regulating RECK gene expression and its potential involvement in liver metabolic processes.

Main Methods:

  • In vivo and in vitro experiments using FXR agonists.
  • Analysis of RECK mRNA and protein expression.
  • Identification of FXR binding sites on the RECK gene promoter region.
  • Studies using a methionine and choline-deficient diet model.

Main Results:

  • RECK was identified as a novel target gene of FXR in mouse liver.
  • FXR agonists significantly increased hepatic RECK mRNA and protein levels.
  • FXR directly binds to a response element in intron 1 of the mouse RECK gene.
  • FXR activation reversed RECK downregulation in mice fed a methionine and choline-deficient diet.

Conclusions:

  • RECK is a novel transcriptional target of FXR in the mouse liver.
  • FXR plays a role in regulating RECK expression, contributing to liver metabolic regulation.
  • These findings provide insights into the broader functions of FXR in hepatic physiology.
Keywords:
FBSFXRFarnesoid X receptorMCDMMPsPEPCKPrimary hepatocytesRECKRXRαSHPSREBP-1cTransactivationfarnesoid X receptorfetal bovine serummatrix metalloproteinasesmethionine and choline deficientphosphoenolpyruvate carboxykinaseretinoid X receptor αreversion-inducing cysteine rich protein with Kazal motifssmall heterodimer partnersterol regulatory element-binding protein-1c

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