Receptor-mediated induction of aminopeptidase A (APA) of human glomerular epithelial cells (HGEC) by glucocorticoids

Membrane-bound peptidases are critical regulators of peptide hormones. We therefore characterized aminopeptidase A (APA) activity in human glomerular epithelial cells (HGEC) and studied the control of its expression. APA, which splits off the N-terminal Asp from angiotensin II (AII), was present at...

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Bibliographic Details
Published in:FEBS letters 1991-12, Vol.294 (3), p.171-174
Main Authors: Stefanovic, V., Vlahovic, P., Ardaillou, N., Ardaillou, R.
Format: Article
Language:English
Subjects:
Aldosterone - pharmacology
Aminopeptidase A
Aminopeptidases - antagonists & inhibitors
Aminopeptidases - biosynthesis
Analytical, structural and metabolic biochemistry
Angiotensin II
Angiotensin II - metabolism
Anti-Bacterial Agents
Biological and medical sciences
Calcium - pharmacology
Cycloheximide - pharmacology
Dactinomycin - pharmacology
Dexamethasone - pharmacology
Enzyme Induction - drug effects
Enzymes and enzyme inhibitors
Epithelium - enzymology
Fundamental and applied biological sciences. Psychology
Glomerular epithelial cells
Glucocorticoids
Glucocorticoids - pharmacology
Glutamyl Aminopeptidase
Humans
Hydrolases
Kidney Glomerulus - enzymology
Mifepristone - pharmacology
Oligopeptides - pharmacology
Peptides
Receptors, Glucocorticoid - physiology
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Summary:Membrane-bound peptidases are critical regulators of peptide hormones. We therefore characterized aminopeptidase A (APA) activity in human glomerular epithelial cells (HGEC) and studied the control of its expression. APA, which splits off the N-terminal Asp from angiotensin II (AII), was present at the surface of HGECs (55% of the total enzyme). APA activity was calcium-dependent and was inhibited by amastatin. Treatment of HGECs by dexamethasone (DEX) increased ecto-APA activity in a dose- and time-dependent manner. Maximal increase of APA activity (× 2) occurred after treatment with 0.5 μM DEX for 5 days. Higher concentrations (1·10 μM) of aldosterone (ALD) stimulated APA activity to a lesser extent (× 1.25). Actinomycin D and cycloheximide prevented and RU 38486, a glucocorticoid receptor antagonist, suppressed the DEX-induced increase in APA activity. These results indicate that AII availability at glomerular receptor sites may be reduced by DEX and suggest a role for glucocorticoids in AII-dependent changes of glomerular filtration rate.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(91)80661-L