Receptor-mediated induction of human glomerular epithelial cell alkaline phosphodiesterase I by glucocorticoids

Alkaline phosphodiesterase I was demonstrated in human glomerular mesangial cells (HGEC) as an ectoenzyme. Treatment of HGEC by dexamethasone increased surface phosphodiesterase I activity in a dose- and time-dependent manner. Maximal increase of phosphodiesterase I activity, about twice, occurred a...

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Bibliographic Details
Published inArchives of physiology and biochemistry Vol. 103; no. 4; p. 427
Main Authors Stefanović, V, Djordjević, V, Mitić, M
Format Journal Article
LanguageEnglish
Published England 1995
Subjects
Cells, Cultured
Cycloheximide - pharmacology
Dexamethasone - pharmacology
Enzyme Induction
Epithelial Cells
Epithelium - drug effects
Epithelium - enzymology
Glomerular Mesangium - cytology
Glomerular Mesangium - drug effects
Glomerular Mesangium - enzymology
Hormone Antagonists - pharmacology
Humans
Mifepristone - pharmacology
Phosphodiesterase I
Phosphoric Diester Hydrolases - biosynthesis
Protein Synthesis Inhibitors - pharmacology
Receptors, Glucocorticoid - antagonists & inhibitors
Receptors, Glucocorticoid - physiology
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Summary:Alkaline phosphodiesterase I was demonstrated in human glomerular mesangial cells (HGEC) as an ectoenzyme. Treatment of HGEC by dexamethasone increased surface phosphodiesterase I activity in a dose- and time-dependent manner. Maximal increase of phosphodiesterase I activity, about twice, occurred after treatment with 5 microM dexamethasone for 6 days. Cycloheximide prevented and RU 38486, a glucocorticoid receptor antagonist, suppressed the dexamethasone induced increase in phosphodiesterase I activity. This study shows that HGEC have a surface phosphodiesterase I controlled by glucocorticoids through a receptor-mediated mechanism.
ISSN:1381-3455
DOI:10.3109/13813459509047133