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Estrogen activates endothelial exocytosis.

Christine S Kim1, Kyungmoo Yea1, Craig N Morrell2

  • 1Department of New Biology, DGIST, Daegu, 42988, South Korea.

Biochemical and Biophysical Research Communications
|April 25, 2021
PubMed
Summary

Estrogen therapy can increase the risk of blood clots by triggering endothelial exocytosis via the ERα-MAP kinase pathway. This non-genomic mechanism contributes to vascular inflammation and thrombosis in post-menopausal women.

Keywords:
Endothelial cellsEstrogenExocytosisPlateletThromboembolism

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Area of Science:

  • Endocrinology
  • Vascular Biology
  • Cellular Biology

Background:

  • Estrogen therapy is widely used for post-menopausal symptoms and osteoporosis prevention.
  • However, estrogen therapy is associated with an increased risk of venous thromboembolic events.
  • The underlying mechanisms linking estrogen to thrombosis remain largely unknown.

Purpose of the Study:

  • To elucidate the molecular pathways through which estrogen increases the risk of vascular thrombosis.
  • To investigate the role of endothelial exocytosis in estrogen-mediated thrombosis.
  • To identify the specific estrogen receptor and signaling pathways involved.

Main Methods:

  • Stimulation of endothelial cells with 17β-estradiol (E2) and measurement of Weibel-Palade body (WPB) exocytosis.
  • Use of estrogen receptor agonists (PPT, DPN) and antagonists (ICI-182,780).
  • Gene silencing of ERα and inhibition of MAP kinase pathways (ERK, p38).
  • Assessment of platelet adhesion to endothelial cells ex vivo.

Main Results:

  • Exogenous 17β-estradiol (E2) stimulated endothelial exocytosis, releasing von Willebrand factor (vWF) and IL-8.
  • The estrogen receptor alpha (ERα) mediated E2-induced vWF release, while ERβ did not.
  • E2-induced exocytosis was rapid, non-genomic, and dependent on the MAP kinase pathway (ERK/p38).
  • E2 treatment enhanced platelet adhesion to endothelial cells ex vivo.

Conclusions:

  • Estrogen activates endothelial exocytosis non-genomically through the ERα-MAP kinase pathway.
  • This mechanism contributes to vascular inflammation and thrombosis.
  • Adverse cardiovascular effects should be considered before initiating menopausal hormone therapy.