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Related Experiment Videos

ERbeta has nongenomic action in caveolae.

Ken L Chambliss1, Ivan S Yuhanna, Richard G W Anderson

  • 1Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. Ken.Chambliss@UTSouthwestern.edu

Molecular Endocrinology (Baltimore, Md.)
|May 1, 2002
PubMed
Summary

Endogenous estrogen receptor beta (ERbeta) mediates rapid endothelial nitric oxide synthase (eNOS) activation via nongenomic signaling in endothelial cell caveolae, independent of ERalpha.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Molecular Signaling

Background:

  • Estrogen receptors (ERalpha and ERbeta) classically function as transcription factors.
  • ERalpha also mediates rapid, nongenomic responses to estradiol (E2), such as endothelial nitric oxide synthase (eNOS) activation.
  • The nongenomic actions of endogenous ERbeta are not well understood.

Purpose of the Study:

  • To investigate the nongenomic actions of endogenous ERbeta in endothelial cells.
  • To determine the subcellular localization of ERbeta's nongenomic function.
  • To elucidate the role of ERbeta in E2-mediated eNOS activation.

Main Methods:

  • Cultured endothelial cells expressing endogenous ERbeta were used.
  • Subcellular localization of ERbeta was examined.

Related Experiment Videos

  • eNOS activation by E2 was measured.
  • ERbeta-selective antagonist (RR-tetrahydrochrysene, THC) was employed.
  • Experiments were conducted in COS-7 cells and isolated endothelial cell plasma membranes and caveolae.

    • Main Results:

    • A subpopulation of ERbeta localized to the endothelial cell plasma membrane.
    • Overexpression of ERbeta enhanced rapid eNOS stimulation by E2.
    • The ERbeta-selective antagonist THC inhibited E2-induced eNOS activation.
    • ERbeta mediated eNOS activation independently of ERalpha in COS-7 cells.
    • ERbeta was detected in endothelial cell caveolae, and THC attenuated E2 stimulation of eNOS within caveolae.

    Conclusions:

    • Endogenous ERbeta possesses nongenomic signaling capacity in endothelial cells.
    • ERbeta mediates rapid eNOS activation through nongenomic mechanisms.
    • Caveolae are a key subcellular locale for ERbeta's nongenomic action and ERbeta-eNOS coupling.