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Induction of plasminogen activator inhibitor 1 gene expression in murine liver by lipopolysaccharide. Cellular localization and role of endogenous tumor necrosis factor-alpha

Academic Article
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Overview

authors

  • Fearns, C.
  • Loskutoff, David J.

publication date

  • February 1997

journal

  • American Journal of Pathology  Journal

abstract

  • We previously demonstrated that lipopolysaccharide (LPS) induces plasminogen activator inhibitor 1 (PAI-1) gene expression primarily in endothelial cells in most organs of the mouse, with maximal induction by 3 hours. Here we show that induction in the liver occurs in a distinctly different pattern. For example, the increase in PAI-1 mRNA in liver was biphasic with an initial peak at 1 to 2 hours and a second peak at 6 to 8 hours. Moreover, in situ hybridization experiments revealed that PAI-1 mRNA was induced in both endothelial cells and hepatocytes. The endothelial cell response was monophasic and maximal between 1 and 4 hours, whereas the hepatocyte response was biphasic, peaking at 2 hours and again at 6 to 8 hours. To determine possible mechanisms involved in the induction of PAI-1 by LPS, we analyzed the tissues for changes in tumor necrosis factor (TNF)-alpha LPS caused a rapid induction of TNF-alpha mRNA in Kupffer cells, detectable within 15 minutes. Pretreatment of mice with anti-TNF antiserum before challenge with LPS reduced the subsequent increase in plasma levels of PAI-1 by 50 to 70% and significantly reduced the level of induction of PAI-1 mRNA in the liver at both early and late times. Pretreatment appeared to inhibit induction primarily within hepatocytes. These results suggest that LPS may induce PAI-1 in endothelial cells and hepatocytes by different mechanisms.

subject areas

  • Animals
  • Female
  • Gene Expression Regulation
  • Lipopolysaccharides
  • Liver
  • Mice
  • Mice, Inbred Strains
  • Plasminogen Activator Inhibitor 1
  • RNA, Messenger
  • Tissue Distribution
  • Tumor Necrosis Factor-alpha
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Identity

PubMed Central ID

  • PMC1858291

International Standard Serial Number (ISSN)

  • 0002-9440

PubMed ID

  • 9033272
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Additional Document Info

start page

  • 579

end page

  • 590

volume

  • 150

issue

  • 2

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