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Estrogen modulates plasminogen promoter activity.

Louise Kobelt1, Jürgen Klammt, Katrin Tefs

  • 1Hospital for Children and Adolescents, Centre for Pediatric Research, University of Leipzig, Germany.

Biochemical and Biophysical Research Communications
|July 23, 2013
PubMed
Summary

Estrogen therapy increases plasminogen (PLG) levels by activating a specific upstream element. This estrogen response element overrides other enhancers, revealing a complex regulation of PLG gene expression.

Keywords:
APO(a)DHDNase hypersensitivityEREEnhancer elementEstrogenEstrogen receptorLp(a)PLGPlasminogenPromoterTSSTranscriptionapolipoprotein(a)estrogen-response elementlipoptrotein(a)plasminogentranscription start site

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Area of Science:

  • Molecular Biology
  • Genetics
  • Endocrinology

Background:

  • Estrogen hormone replacement therapy and oral contraceptives increase plasminogen (PLG) concentrations in women.
  • Plasminogen (PLG) and apolipoprotein(a) [APO(a)] genes are located close together on chromosome 6q26 and share structural homology.
  • Estrogen typically decreases lipoprotein(a) [Lp(a)] levels, contrasting with the observed increase in PLG.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying estrogen-mediated regulation of plasminogen (PLG) gene expression.
  • To identify specific regulatory elements responsive to estrogen in the vicinity of the PLG and APO(a) genes.

Main Methods:

  • Luciferase reporter assays were employed to assess the activity of the PLG core promoter and its regulatory regions.
  • The effects of estrogen on promoter activity were examined using identified enhancer and estrogen response elements.
  • Analysis focused on the intergenic region between the PLG and APO(a) genes.

Main Results:

  • The minimal PLG promoter itself is not directly sensitive to estrogen.
  • An estrogen response element located 11.5 kb upstream significantly enhances PLG promoter activity in an estrogen-dependent manner.
  • Estrogen abrogates the activating effects of two other enhancer elements, including one that regulates APO(a) promoter activity.

Conclusions:

  • Specific estrogen-responsive elements in the PLG gene locus mediate estrogen-dependent transcriptional regulation.
  • Estrogen's effect on PLG expression is complex, involving both activation via specific elements and potential abrogation of other enhancers.
  • These findings provide insights into the gene and tissue-specific regulation of PLG expression, potentially involving unknown accessory factors.