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Protein kinase C activation and calcium mobilization decrease prolactin release from human decidual cells in early

T Kubota1, S Kamada, M Taguchi

  • 1Department of Obstetrics and Gynecology, Tokyo Medical and Dental University, Faculty of Medicine, Japan.

The Journal of Endocrinology
|May 1, 1993
PubMed
Summary
This summary is machine-generated.

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Protein kinase C (PKC) activation and calcium mobilization suppress prolactin release from human decidual cells in early pregnancy. These pathways regulate prolactin secretion without affecting cell proliferation or DNA synthesis.

Area of Science:

  • Reproductive Biology
  • Cell Signaling
  • Endocrinology

Background:

  • Human decidual cells play a crucial role in early pregnancy.
  • Prolactin secretion by decidual cells is essential for maintaining pregnancy.
  • Understanding the regulation of prolactin release is key to reproductive health.

Purpose of the Study:

  • To investigate the role of protein kinase C (PKC) activation in regulating prolactin release.
  • To examine the impact of calcium mobilization on prolactin secretion from decidual cells.
  • To elucidate the signaling pathways involved in prolactin regulation during early pregnancy.

Main Methods:

  • Decidual cells from early pregnancy were cultured.
  • Cells were treated with phorbol myristate acetate (PMA), a PKC activator, and calcium ionophore A23187.

Related Experiment Videos

  • Prolactin levels in the culture medium were measured using enzyme-immunoassay.

    • Main Results:

    • PKC activation by PMA dose-dependently reduced prolactin release.
    • A PKC inhibitor (H7) blocked the effect of PMA on prolactin release.
    • Calcium ionophore A23187 also attenuated prolactin release and enhanced PMA's suppressive effect.
    • PKC activation did not affect cell proliferation, DNA synthesis, inositol phosphate generation, or intracellular calcium levels.

    Conclusions:

    • PKC activation and calcium mobilization are involved in the regulation of prolactin release from human decidual cells.
    • The suppression of prolactin release by PMA is independent of phosphoinositide hydrolysis and intracellular calcium increase.
    • These findings highlight novel regulatory mechanisms for prolactin secretion in early pregnancy.