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This version published online on September 5, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-0538
A more recent version of this article appeared on November 1, 2006
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*Substance via MeSH
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*Cushing's Syndrome

Submitted on March 9, 2006
Accepted on August 30, 2006

Expression of serotonin7 receptor and coupling of ectopic receptors to protein kinase A and ionic currents in ACTH-independent macronodular adrenal hyperplasia causing Cushing's syndrome

Estelle Louiset, Vincent Contesse, Lionel Groussin, Dorthe Cartier, Céline Duparc, Gaëlle Barrande, Jérôme Bertherat, Hubert Vaudry, and Hervé Lefebvre*

INSERM U413, (E.L., V.C., D.C., C.D., H.V., H.L.), Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France; Department of Endocrinology (L.G., J.B.), CHU Cochin & Institut Cochin, INSERM U567, CNRS UMR8104, IFR 116, Université Paris V-René Descartes, 75014 Paris, France, and Department of Endocrinology (G.B.), CH d'Orléans, 45067 Orléans, France

* To whom correspondence should be addressed. E-mail: herve.lefebvre{at}chu-rouen.fr.

Context: In ACTH-independent macronodular adrenal hyperplasia (AIMAH) causing Cushing's syndrome, cortisol secretion is controlled by illegitimate membrane receptors.

Objective: The aim of the present study was to characterize the pharmacological properties and the transduction mechanisms of illegitimate receptors, i.e. receptors for 5-HT, GIP and LH/hCG, expressed by AIMAH tissues to evaluate the role of ectopic receptors in the physiopathology of the Cushing's syndrome.

Design: In vitro studies on cultured adrenal hyperplasia cells.

Setting: University research laboratory.

Patients: AIMAH tissues (H1-H3) removed from three patients previously screened for illegitimate receptors.

Main outcome measure: Steroidogenic and electrical activities of cultured adrenal hyperplasia cells.

Results: In vitro studies showed that the corticotropic effect of 5-HT was mediated by ectopic 5-HT7 receptors in H1 and H2. GIP and hCG stimulated cortisol production via activation of cAMP-dependent protein kinase (PKA) in H2. On the contrary, the PKA inhibitor H-89 did not affect hCG-induced cortisol production in H3. Activation of 5-HT7 or GIP receptors enhanced T-type calcium current in H1 or H2 and H3, respectively. In addition, GIP reduced the amplitude of transient and sustained potassium currents in H2. Conversely, hCG did not modify T-type calcium current in H3.

Conclusions: These data show that, besides their coupling to the cAMP pathway, illegitimate adrenal receptors can activate additional transduction mechanisms, including modulation of membrane channels.
Key words: illegitimate membrane receptor • cortisol • Cushing's syndrome • 5-HT • GIP • LH • PKA • calcium current




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E Louiset, V Contesse, L Groussin, D Cartier, C Duparc, V Perraudin, J Bertherat, and H Lefebvre
Expression of vasopressin receptors in ACTH-independent macronodular bilateral adrenal hyperplasia causing Cushing's syndrome: molecular, immunohistochemical and pharmacological correlates
J. Endocrinol., January 1, 2008; 196(1): 1 - 9.
[Abstract] [Full Text] [PDF]


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