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Related Experiment Video

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Visualizing the Interrenal Steroidogenic Tissue and Its Vascular Microenvironment in Zebrafish

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FGF signalling through Fgfr2 isoform IIIb regulates adrenal cortex development.

Leonardo Guasti¹, W C Candy Sze, Tristan McKay

¹Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, UK.

Molecular and Cellular Endocrinology

|February 5, 2013

Summary

Fibroblast growth factor receptor 2 (Fgfr2) signaling is vital for adrenal gland development. Deleting the Fgfr2 IIIb isoform in mice impairs adrenal growth and alters key gene expression, highlighting capsule-cortex communication importance.

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Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions

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Published on: March 12, 2019

Area of Science:

Endocrinology
Developmental Biology
Molecular Biology

Background:

Developmental signalling pathways regulate adrenal gland formation and maintenance.
Sonic hedgehog (Shh) and Wnt/β-catenin signalling are known to be crucial for adrenal cortex development.
The specific roles of Fibroblast growth factor receptor (Fgfr) signalling in adrenal development require further definition.

Purpose of the Study:

To investigate the role of Fibroblast growth factor receptor (Fgfr) 2 isoforms in adrenal gland development during embryogenesis.
To determine the consequences of specific Fgfr2 isoform deletion on adrenal gland structure and function.

Main Methods:

Analysis of Fgfr2 isoform IIIb and IIIc expression in the adrenal subcapsule during embryogenesis.
Generation of genetically modified mouse models with specific deletion of the Fgfr2 IIIb isoform.
Assessment of adrenal gland growth, morphology, and expression of key developmental and steroidogenic genes (SF1, steroidogenic enzymes, Gli1, Dlk1).

Main Results:

Fgfr2 IIIb and IIIc isoforms are primarily expressed in the adrenal subcapsule during embryogenesis.
Specific deletion of the Fgfr2 IIIb isoform leads to impaired adrenal development, characterized by reduced adrenal growth and hypoplasia.
Deletion of Fgfr2 IIIb results in altered expression of SF1 and steroidogenic enzymes, disorganized adrenal capsules with retained Gli1 expression, and loss of Dlk1 expression.
Fgfr2 ligands are detected in both the adrenal capsule and cortex.

Conclusions:

The Fgfr2 IIIb isoform plays a critical role in embryonic adrenal gland development.
Fgfr2 signalling is essential for maintaining normal adrenal gland growth, capsule structure, and the expression of key regulatory and steroidogenic genes.
Interactions between the adrenal capsule and cortex, mediated by Fgfr2 ligands, are crucial for proper adrenal development.