Abstract
We show here for the first time that sphingosine-1-phosphate (Sph-1-P) stimulates cortisol secretion in zona fasciculata cells of bovine adrenal glands. This effect was dependent upon protein kinase C (PKC) and extracellular Ca2+, and was inhibited by pertussis toxin. Sph-1-P activated phospholipase D (PLD) through a pertussis toxin-sensitive mechanism, also involving extracellular Ca2+ and PKC. Primary alcohols, which attenuate formation of phosphatidic acid (the product of PLD), and cell-permeable ceramides, which inhibit PLD, blocked Sph-1-P-induced cortisol secretion. In conclusion, Sph-1-P stimulates cortisol secretion through a mechanism involving Gi/o protein-coupled receptors, extracellular Ca2+, PKC and PLD.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium / metabolism
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Cattle
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Cells, Cultured
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Ceramides / pharmacology
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Chelating Agents / pharmacology
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Enzyme Activation / drug effects
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GTP-Binding Protein alpha Subunits, Gi-Go / metabolism
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Heterotrimeric GTP-Binding Proteins / metabolism
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Hydrocortisone / metabolism*
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Lipids / pharmacology
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Lysophospholipids*
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Pertussis Toxin / pharmacology
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Phosphatidic Acids / biosynthesis
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Phospholipase D / antagonists & inhibitors
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Phospholipase D / metabolism
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Protein Kinase C / metabolism
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Sphingosine / analogs & derivatives*
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Sphingosine / pharmacology*
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Zona Fasciculata / cytology
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Zona Fasciculata / drug effects*
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Zona Fasciculata / metabolism*
Substances
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Ceramides
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Chelating Agents
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Lipids
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Lysophospholipids
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Phosphatidic Acids
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sphingosine 1-phosphate
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Pertussis Toxin
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Protein Kinase C
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Phospholipase D
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GTP-Binding Protein alpha Subunits, Gi-Go
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Heterotrimeric GTP-Binding Proteins
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Sphingosine
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Calcium
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Hydrocortisone