Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

Interleukin-6-induced plasminogen gene expression in murine hepatocytes is mediated by transcription factor CCAAT/enhancer binding protein beta (C/EBP beta)

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Bannach, F. G.
  • Gutierrez-Fernandez, A.
  • Parmer, R. J.
  • Miles, Lindsey

publication date

  • 2004

journal

  • Journal of Thrombosis and Haemostasis  Journal

abstract

  • An emerging area of research has demonstrated that plasminogen functions in the acute-phase response to tissue injury, neoplastic growth or infection. We have previously shown that the acute-phase mediator, interleukin (IL)-6, increases circulating plasminogen levels via upregulation of plasminogen promoter activity. We also identified a putative IL-6 responsive element (nt -791 to -783; IL6-RE) in the plasminogen gene that is required for maximal stimulation of promoter activity by IL-6. For the present study, we investigated the transcription factors and signaling pathway mediating the response of the plasminogen gene to IL-6. In electrophoretic mobility shift assays (EMSAs), a radiolabeled oligonucleotide IL6-RE probe formed specific complexes with nuclear proteins from untreated hepatocytic cells. The extent of complex formation was markedly increased using nuclear proteins from IL-6-treated cells. Complex formation was abolished by an oligonucleotide with the consensus CCAAT/enhancer binding protein (C/EBP) sequence. Furthermore, complexes were supershifted by antibodies to C/EBPbeta. Treatment of Hepa 1-6 cells with the mitogen-activated protein kinase (MAPK) inhibitor, PD-98059, inhibited IL-6-stimulated plasminogen promoter activity. These results suggest that transcription factor C/EBPbeta and the MAPK pathway play key roles in the response of the plasminogen gene to IL-6, thus elucidating a major mechanism by which the plasminogen system is upregulated to perform its crucial functions in the acute-phase response.

subject areas

  • Acute-Phase Reaction
  • Animals
  • Base Sequence
  • Binding Sites
  • CCAAT-Enhancer-Binding Proteins
  • Cell Line, Tumor
  • Cell Nucleus
  • Enzyme Inhibitors
  • Flavonoids
  • Gene Expression Regulation
  • Genes, Reporter
  • Hepatocytes
  • Interleukin-6
  • Luciferases
  • MAP Kinase Signaling System
  • Mice
  • Models, Genetic
  • Molecular Sequence Data
  • Oligonucleotides
  • Plasmids
  • Plasminogen
  • Promoter Regions, Genetic
  • Protein Binding
  • Sequence Homology, Nucleic Acid
  • Signal Transduction
  • Transcription, Genetic
  • Transfection
  • Up-Regulation
scroll to property group menus

Research

keywords

  • C/EBP beta
  • interleukin-6
  • plasminogen
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 1538-7933

Digital Object Identifier (DOI)

  • 10.1111/j.1538-7836.2004.01022.x

PubMed ID

  • 15613028
scroll to property group menus

Additional Document Info

start page

  • 2205

end page

  • 2212

volume

  • 2

issue

  • 12

©2019 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support