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Updated: Jul 31, 2026
08:28
Zebrafish Brain Ventricle Injection
Published on: April 6, 2009
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Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafish
Marlene Trindade1,2, Nádia Silva1, Joana Rodrigues1
1Algarve Biomedical Center-Research Institute, Universidade do Algarve, Faro, Portugal.
Communications Biology
|July 2, 2025
Summary
Maternal thyroid hormone (MTH) transport via MCT8 is crucial for hindbrain development. This study reveals MTH regulates neuroprogenitor cells to guide blood vessel formation in the zebrafish hindbrain.
Area of Science:
- Developmental Biology
- Neuroscience
- Endocrinology
Background:
- Thyroid hormone (TH) signaling is essential for neurodevelopment.
- Mutations in the monocarboxylate transporter 8 (SLC16A2, MCT8) cause Allan-Herndon-Dudley Syndrome (AHDS), impairing brain development.
- MCT8 is the primary TH transporter in the embryonic brain.
Purpose of the Study:
- To investigate the role of maternal T3 (MT3) and MCT8 in hindbrain vasculature development.
- To elucidate the cellular source of vegfaa and its regulation by MT3 in the hindbrain.
Main Methods:
- Utilized zebrafish Mct8 knockdown (KD) and knockout (KO) models.
- Analyzed hindbrain vasculature development and vegfaa expression.
- Investigated the role of pax6a+ neuroprogenitor cells (NPCs) in central arteries (CtAs) ingression.
Main Results:
- Maternal T3 (MT3) regulates hindbrain vegfaa expression.
- Hindbrain neurons are not the source of vegfaa; pax6a+ NPCs instruct CtAs ingression.
- MCT8 is critical for MT3-dependent hindbrain vasculature development.
Conclusions:
- MT3, acting through MCT8, is a key regulator of hindbrain vasculature development.
- Pax6a+ neuroprogenitor cells mediate the effects of MT3 on blood vessel formation.
- This study identifies a novel mechanism linking maternal thyroid hormone to neurovascular development.
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