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Updated: Jun 4, 2026
08:33
An Ex vivo Culture System to Study Thyroid Development
Published on: June 6, 2014
Hes1 is required for appropriate morphogenesis and differentiation during mouse thyroid gland development
Aurore Carre1, Latif Rachdi, Elodie Tron
1INSERM U845, Université Paris-Descartes, Paris, France.
Plos One
|March 3, 2011
Summary
Hes1 is crucial for thyroid development, controlling progenitor cell numbers and ensuring proper thyroid hormone and calcitonin production. Its absence leads to smaller thyroids and impaired endocrine function.
Area of Science:
- Endocrinology
- Developmental Biology
- Molecular Genetics
Background:
- Notch signalling and its target Hes1 regulate endocrine development.
- Hes1 is expressed in the thyroid and influences the sodium iodide symporter (Nis).
- Understanding Hes1's role is key to thyroid development and function.
Purpose of the Study:
- To investigate the role of Hes1 in mouse thyroid morphology and function.
- To analyze the impact of Hes1 deficiency on thyroid progenitor cells and differentiation.
- To elucidate Hes1's contribution to endocrine gland development.
Main Methods:
- Studied thyroid development in Hes1-deficient (Hes1(-/-)) and wild-type mice from embryonic day 9.5 to 16.5.
- Assessed thyroid morphology, progenitor cell numbers (Nkx2-1), cell cycle inhibitor p57, and proliferation.
- Quantified labelling areas for T4, calcitonin, and sodium iodide symporter (Nis) in developing thyroids.
Main Results:
- Hes1(-/-) embryos exhibited fewer Nkx2-1-positive progenitor cells and significantly smaller thyroid surface areas.
- Thyroid anlage fusion was delayed in Hes1(-/-) embryos.
- Hypoplastic Hes1(-/-) thyroids showed reduced T4, calcitonin, and Nis expression, indicating impaired endocrine function.
Conclusions:
- Hes1 controls the number of thyrocyte and C-cell progenitors through a p57-independent mechanism.
- Hes1 is essential for the adequate differentiation and endocrine function of thyroid cells.
- Hes1 plays a dual role in thyroid development, impacting both progenitor cell numbers and functional maturation.
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