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cGMP-dependent ADP depolymerization of actin mediates estrogen increase in cervical epithelial permeability.

G I Gorodeski1

  • 1Departments of Reproductive Biology and Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA. gig@po.cwru.edu

American Journal of Physiology. Cell Physiology
|November 18, 2000
PubMed
Summary

Estrogen, nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) promote actin depolymerization in cervical cells. This process involves NO-induced, cGMP-dependent protein kinase enhancing actin ADP-ribosylation.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Molecular Mechanisms

Background:

  • Estrogen influences cervical mucus secretion, a process linked to cytoskeletal changes.
  • The precise molecular pathways of estrogen's action on the cytoskeleton remain incompletely understood.

Purpose of the Study:

  • To elucidate the molecular mechanism by which estrogen affects the actin cytoskeleton in human cervical epithelial cells.
  • To investigate the roles of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) in estrogen-mediated cytoskeletal regulation.

Main Methods:

  • Human cervical epithelial cells were treated with 17beta-estradiol, sodium nitroprusside (SNP), or 8-bromoguanosine 3', 5'-cyclic monophosphate (8-Br-cGMP).
  • Inhibitors including tamoxifen, LY-83583 (guanylate cyclase inhibitor), and KT-5823 (cGMP-dependent protein kinase inhibitor) were used to block specific pathways.

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  • Changes in monomeric G-actin and polymerized F-actin were assessed, along with paracellular permeability and protein phosphorylation.

    • Main Results:

    • 17beta-estradiol, SNP, and 8-Br-cGMP treatment led to increased G-actin and decreased F-actin, indicating actin depolymerization.
    • Estrogen's effects were inhibited by tamoxifen, LY-83583, and KT-5823, suggesting involvement of NO and cGMP signaling.
    • SNP and 8-Br-cGMP also induced actin depolymerization, with specific inhibitor profiles revealing distinct pathway contributions.
    • These agents attenuated phosphorylation of [(32)P]adenylate NAD in vitro, with differential blockade by inhibitors.

    Conclusions:

    • Estrogen, NO, and cGMP collectively stimulate actin depolymerization in cervical epithelial cells.
    • A proposed mechanism involves NO-mediated activation of cGMP-dependent protein kinase, which augments ADP-ribosylation of monomeric actin.
    • These findings provide insight into the molecular regulation of cytoskeletal dynamics by hormones and signaling molecules.