Receptor-mediated induction of human dermal fibroblast ectoaminopeptidase N by glucocorticoids

Aminopeptidase N was demonstrated in human dermal fibroblasts as an ectoenzyme. The enzyme has wide substrate specificity, with a K(m) of 0.63 mM and Vmax of 338 nmol min-1 mg-1. Addition of fetal calf serum to the culture medium increased aminopeptidase N activity up to 63% by 10% serum in a 48-h c...

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Bibliographic Details
Published in:Cellular and molecular life sciences : CMLS 1998-06, Vol.54 (6), p.614-617
Main Authors: Stefanovic, V, Vlahovic, P, Mitic-zlatkovic, M
Format: Article
Language:English
Subjects:
Biosynthesis
CD13 Antigens - metabolism
Culture Media - pharmacology
Cycloheximide - pharmacology
Dactinomycin - pharmacology
Dexamethasone - pharmacology
Enzymes
Fibroblasts
Gene Expression Regulation, Enzymologic - drug effects
Glucocorticoids - pharmacology
Hormones
Humans
Kinetics
Mifepristone - pharmacology
Molecular biology
Protein synthesis
Proteins
Receptors, Cell Surface - physiology
Receptors, Glucocorticoid - metabolism
Skin - enzymology
Substrate Specificity
Up-Regulation - physiology
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Summary:Aminopeptidase N was demonstrated in human dermal fibroblasts as an ectoenzyme. The enzyme has wide substrate specificity, with a K(m) of 0.63 mM and Vmax of 338 nmol min-1 mg-1. Addition of fetal calf serum to the culture medium increased aminopeptidase N activity up to 63% by 10% serum in a 48-h culture. Treatment of fibroblasts by dexamethasone increased ectoaminopeptidase N activity in a dose- and time-dependent manner. Maximal increase of aminopeptidase N occurred after treatment with 1 microM dexamethasone for 3 days. Actinomycin D, a blocker of RNA synthesis, and cycloheximide, an inhibitor of protein synthesis, did not alter basal aminopeptidase N activity. However, they prevented stimulation by dexamethasone. RU 38486, a glucocorticoid receptor antagonist, suppressed the dexamethasone-induced increase in aminopeptidase N activity. This study shows that human dermal fibroblasts contain ectoaminopeptidase N controlled by glucocorticoids through a receptor-mediated mechanism.
ISSN:1420-682X
1420-9071
DOI:10.1007/s000180050189