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FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development

Developmental signalling pathways are implicated in the formation and maintenance of the adrenal gland, but their roles are currently not well defined. In recent years it has emerged that Sonic hedgehog (Shh) and Wnt/β catenin signalling are crucial for the growth and development of the adrenal cort...

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Detalles Bibliográficos
Autores principales: Guasti, Leonardo, Candy Sze, W.C., McKay, Tristan, Grose, Richard, King, Peter J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: North Holland Publishing 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650577/
https://www.ncbi.nlm.nih.gov/pubmed/23376610
http://dx.doi.org/10.1016/j.mce.2013.01.014
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author Guasti, Leonardo
Candy Sze, W.C.
McKay, Tristan
Grose, Richard
King, Peter J.
author_facet Guasti, Leonardo
Candy Sze, W.C.
McKay, Tristan
Grose, Richard
King, Peter J.
author_sort Guasti, Leonardo
collection PubMed
description Developmental signalling pathways are implicated in the formation and maintenance of the adrenal gland, but their roles are currently not well defined. In recent years it has emerged that Sonic hedgehog (Shh) and Wnt/β catenin signalling are crucial for the growth and development of the adrenal cortex. Here we demonstrate that Fibroblast growth factor receptor (Fgfr) 2 isoforms IIIb and IIIc are expressed mainly in the adrenal subcapsule during embryogenesis and that specific deletion of the Fgfr2 IIIb isoform impairs adrenal development, causing reduced adrenal growth and impaired expression of SF1 and steroidogenic enzymes. The hypoplastic adrenals also have thicker, disorganised capsules which retain Gli1 expression but no longer express Dlk1. Fgfr2 ligands were detected in both the capsule and the cortex, suggesting the importance of signalling between the capsule and the cortex in adrenal development.
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spelling pubmed-36505772013-05-22 FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development Guasti, Leonardo Candy Sze, W.C. McKay, Tristan Grose, Richard King, Peter J. Mol Cell Endocrinol Article Developmental signalling pathways are implicated in the formation and maintenance of the adrenal gland, but their roles are currently not well defined. In recent years it has emerged that Sonic hedgehog (Shh) and Wnt/β catenin signalling are crucial for the growth and development of the adrenal cortex. Here we demonstrate that Fibroblast growth factor receptor (Fgfr) 2 isoforms IIIb and IIIc are expressed mainly in the adrenal subcapsule during embryogenesis and that specific deletion of the Fgfr2 IIIb isoform impairs adrenal development, causing reduced adrenal growth and impaired expression of SF1 and steroidogenic enzymes. The hypoplastic adrenals also have thicker, disorganised capsules which retain Gli1 expression but no longer express Dlk1. Fgfr2 ligands were detected in both the capsule and the cortex, suggesting the importance of signalling between the capsule and the cortex in adrenal development. North Holland Publishing 2013-05-22 /pmc/articles/PMC3650577/ /pubmed/23376610 http://dx.doi.org/10.1016/j.mce.2013.01.014 Text en © 2013 Elsevier Ireland Ltd. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
spellingShingle Article
Guasti, Leonardo
Candy Sze, W.C.
McKay, Tristan
Grose, Richard
King, Peter J.
FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development
title FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development
title_full FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development
title_fullStr FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development
title_full_unstemmed FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development
title_short FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development
title_sort fgf signalling through fgfr2 isoform iiib regulates adrenal cortex development
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650577/
https://www.ncbi.nlm.nih.gov/pubmed/23376610
http://dx.doi.org/10.1016/j.mce.2013.01.014
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