MRE-binding transcription factor-1 is activated during endotoxemia: a central role for metallothionein

Toxicol Lett. 2002 Mar 24;129(1-2):77-84. doi: 10.1016/s0378-4274(01)00473-8.

Abstract

Endotoxin (LPS) has been established to induce hepatic metallothionein (MT), but the specific role of MT remains unknown. In this study, we examined whether MT can modulate MTF-1 activity during endotoxemia. Treatment with IL-6, the main mediator of MT induction during endotoxemia, enhanced the expression of the MRE(d)-driven reporter gene. MTF-1 DNA-binding activity was increased 16-24 h after LPS administration in wild-type mice, while no such activation was observed in MT-null mice during the same period. The expression of alpha(1)-acid glycoprotein (AGP) mRNA, an RNA regulated by MTF-1, was lower in MT-null than in wild-type mice. Our results suggested that MTF-1 was activated during endotoxemia. MT can act as an activator of MTF-1, and MT can induce MTF-1 targeted gene expression during endotoxemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DNA / metabolism
  • DNA-Binding Proteins
  • Endotoxemia / metabolism*
  • Female
  • Humans
  • Interleukin-6 / pharmacology
  • Lipopolysaccharides / toxicity
  • Metallothionein / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred ICR
  • Orosomucoid / genetics
  • RNA, Messenger / analysis
  • Response Elements
  • Transcription Factor MTF-1
  • Transcription Factors / metabolism*
  • Transcription, Genetic / drug effects

Substances

  • DNA-Binding Proteins
  • Interleukin-6
  • Lipopolysaccharides
  • Orosomucoid
  • RNA, Messenger
  • Transcription Factors
  • DNA
  • Metallothionein