Abstract
We have previously reported that parathyroid hormone (PTH) has specific effects on a human umbilical vein endothelial cell line. Further studies were performed to characterize the signaling cascades initiated by PTH. We report that PTH induced the appearance of voltage sensitive calcium channels. Furthermore, PTH increased ceramide but not diacylglycerol content. Since elevations in [Ca(2+)](i) and phospholipid turnover are signals for the activation of protein kinase C (PKC), the cells were screened for PKC isoforms. PTH induced a redistribution of the PKCepsilon to the particulate fractions of cell homogenates. In summary, PTH induced PKC translocation through a calcium-phospholipid pathway in an endothelial cell line.
MeSH terms
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Aequorin / pharmacology
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Barium / pharmacology
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Calcium / metabolism
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Calcium Channels / metabolism
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Cell Line
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Ceramides / metabolism
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Diglycerides / metabolism
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Diglycerides / pharmacology
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Dose-Response Relationship, Drug
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism*
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Humans
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Parathyroid Hormone / pharmacology*
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Patch-Clamp Techniques
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Peptides / pharmacology*
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Phospholipids / metabolism
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Potassium / pharmacology
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Protein Isoforms
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Protein Kinase C / biosynthesis
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Protein Kinase C / chemistry
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Protein Transport
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Signal Transduction* / drug effects
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Time Factors
Substances
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Calcium Channels
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Ceramides
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Diglycerides
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Parathyroid Hormone
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Peptides
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Phospholipids
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Protein Isoforms
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Barium
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Aequorin
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Protein Kinase C
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Potassium
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Calcium