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Sphingosine-1-phosphate stimulates cortisol secretion.

Miriam Rábano1, Ana Peña, Leyre Brizuela

  • 1Department of Biochemistry and Molecular Biology, Faculty of Sciences, University of the Basque Country, P.O. Box 644, 48080 Bilbao, Spain.

FEBS Letters
|February 1, 2003
PubMed
Summary

Sphingosine-1-phosphate (Sph-1-P) stimulates cortisol secretion in adrenal cells. This process involves protein kinase C (PKC), extracellular calcium, and phospholipase D (PLD) activation via Gi/o protein-coupled receptors.

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Area of Science:

  • Endocrinology
  • Cell Signaling
  • Adrenal Physiology

Background:

  • The adrenal cortex, specifically the zona fasciculata, is responsible for cortisol production.
  • Intracellular signaling pathways regulating steroidogenesis are complex and not fully elucidated.
  • Sphingosine-1-phosphate (Sph-1-P) is a bioactive lipid mediator with diverse cellular functions.

Purpose of the Study:

  • To investigate the effect of sphingosine-1-phosphate (Sph-1-P) on cortisol secretion.
  • To elucidate the signaling mechanisms underlying Sph-1-P-induced cortisol release in bovine adrenal cells.

Main Methods:

  • Primary culture of bovine adrenal zona fasciculata cells.
  • Measurement of cortisol secretion in response to Sph-1-P stimulation.
  • Investigation of the roles of protein kinase C (PKC), extracellular calcium (Ca2+), pertussis toxin-sensitive G proteins, and phospholipase D (PLD) in the signaling pathway.

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Main Results:

  • Sphingosine-1-phosphate (Sph-1-P) significantly stimulated cortisol secretion.
  • This stimulation was dependent on extracellular Ca2+, protein kinase C (PKC) activation, and a pertussis toxin-sensitive mechanism.
  • Sph-1-P activated phospholipase D (PLD), and inhibition of PLD or its product, phosphatidic acid, blocked cortisol secretion.

Conclusions:

  • Sphingosine-1-phosphate (Sph-1-P) acts as a novel stimulator of cortisol secretion in the zona fasciculata.
  • The signaling pathway involves Gi/o protein-coupled receptors, extracellular Ca2+, PKC, and PLD.
  • These findings reveal a new regulatory pathway for adrenal steroidogenesis.