دورية أكاديمية
Topical Mineralocorticoid Receptor Blockade Limits Glucocorticoid-Induced Epidermal Atrophy in Human Skin
العنوان: | Topical Mineralocorticoid Receptor Blockade Limits Glucocorticoid-Induced Epidermal Atrophy in Human Skin |
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المؤلفون: | Maubec, Eve, Laouenan, Cedric, Deschamps, Lydia, van Tuan, Nguyen, Scheer-Senyarich, Isabelle, Wackenheim-Jacobs, Anne-Catherine, Steff, Maud, Duhamel, Stephanie, Tubiana, Sarah, Brahimi, Nesrine, Leclerc-Mercier, Stephanie, Crickx, Beatrice, Perret, Claudine, Aractingi, Selim, Escoubet, Brigitte, Duval, Xavier, Arnaud, Philippe, Jaisser, Frederic, Mentre, France, Farman, Nicolette |
المساهمون: | AP-HP - Hôpital Bichat - Claude Bernard Paris, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche Saint-Antoine (UMRS893), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École Pratique des Hautes Études (EPHE), Université Paris Sciences et Lettres (PSL)-Université Paris Sciences et Lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Site Tarnier (hôpital Cochin) - APHP, Hôpital Bichat / Centre d'Investigation Clinique 007, Assistance Publique-Hopitaux de Paris, Unité de Technologies Chimiques et Biologiques pour la Santé (UTCBS - UM 4 (UMR 8258 / U1022)), Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris Sciences et Lettres (PSL)-Université Paris Sciences et Lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie - CNRS Chimie (INC-CNRS)-Centre National de la Recherche Scientifique (CNRS) |
المصدر: | ISSN: 0022-202X. |
بيانات النشر: | HAL CCSD Nature Publishing Group |
سنة النشر: | 2015 |
مصطلحات موضوعية: | DERMAL FIBROBLASTS, HEART-FAILURE, ALDOSTERONE, SPIRONOLACTONE, EXPRESSION, CORTISOL, MICE, DIFFERENTIATION, CORTICOSTERONE, MORTALITY, [SDV.SP.PG]Life Sciences [q-bio]/Pharmaceutical sciences/Galenic pharmacology, [SDV.BIO]Life Sciences [q-bio]/Biotechnology |
الوصف: | International audience ; A major deleterious side effect of glucocorticoids is skin atrophy. Glucocorticoids activate the glucocorticoid and the mineralocorticoid (MR) receptor, both present in the epidermis. We hypothesized that glucocorticoid-induced epidermal atrophy may be related to inappropriate occupancy of MR by glucocorticoids. We evaluated whether epidermal atrophy induced by the topical glucocorticoid clobetasol could be limited by coadministration of MR antagonist. In cultured human skin explants, the epidermal atrophy induced by clobetasol was significantly limited by MR antagonism (canrenoate and eplerenone). Blockade of the epithelial sodium channel ENaC by phenamil was also efficient, identifying a role of MR-ENaC cascade in keratinocytes, acting through restoration of clobetasol-induced impairment of keratinocyte proliferation. In the SPIREPI randomized double-blind controlled trial, gels containing clobetasol, the MR antagonist spironolactone, both agents, or placebo were applied on four zones of the forearms of 23 healthy volunteers for 28 days. Primary outcome was histological thickness of the epidermis with clobetasol alone or clobetasol+spironolactone. Spironolactone alone did not affect the epidermal thickness but coapplication of clobetasol and spironolactone significantly limited clobetasol-induced atrophy and was well tolerated. Altogether, these findings identify MR as a factor regulating epidermal homeostasis and suggest that topical MR blockade could limit glucocorticoid-induced epidermal atrophy. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
ردمك: | 978-0-00-356180-7 0-00-356180-1 |
العلاقة: | hal-03292690; https://cnrs.hal.science/hal-03292690Test; WOS: 000356180100017 |
DOI: | 10.1038/jid.2015.44 |
الإتاحة: | https://doi.org/10.1038/jid.2015.44Test https://cnrs.hal.science/hal-03292690Test |
رقم الانضمام: | edsbas.E22333E5 |
قاعدة البيانات: | BASE |
ردمك: | 9780003561807 0003561801 |
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DOI: | 10.1038/jid.2015.44 |