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Hauptverfasser: Trindade, Marlene, Silva, Nádia, Rodrigues, Joana, Kawakami, Koichi, Campinho, Marco A
Format: Artículo científico
Sprache:en
Veröffentlicht: Communications biology 2025
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Online-Zugang:https://pubmed.ncbi.nlm.nih.gov/40593336/
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author Trindade, Marlene
Silva, Nádia
Rodrigues, Joana
Kawakami, Koichi
Campinho, Marco A
author_facet Trindade, Marlene
Silva, Nádia
Rodrigues, Joana
Kawakami, Koichi
Campinho, Marco A
Trindade, Marlene
Silva, Nádia
Rodrigues, Joana
Kawakami, Koichi
Campinho, Marco A
collection PubMed - marine biology
contents Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafish. Trindade, Marlene Silva, Nádia Rodrigues, Joana Kawakami, Koichi Campinho, Marco A Animals Zebrafish Rhombencephalon Zebrafish Proteins Monocarboxylic Acid Transporters Thyroid Hormones Gene Expression Regulation, Developmental Symporters Female Vascular Endothelial Growth Factor A Thyroid hormone (TH) signaling is important and necessary for proper neurodevelopment. Inadequate levels of maternally derived THs (MTH) supply affect target gene expression profiles, which are fundamental for the brain's normal growth, maturation, and function. The monocarboxylate transporter 8 (SLC16A2, MCT8) is the main TH transporter present in the brain during embryonic development, and mutations in this transporter lead to a rare and debilitating human condition known as the Allan-Herndon-Dudley Syndrome (AHDS). This mutation affects the capacity for intracellular transport of the hormone, leading to impaired brain development that constitutes the main pathophysiological basis of AHDS. Like humans, zebrafish embryos express slc16a2 that transports exclusively T3 at zebrafish physiological temperature. Studies in zebrafish Mct8 knockdown (KD) models found impaired hindbrain vasculature development. Here, using zebrafish Mct8 KD and knockout (KO) models, we shed light on the maternal T3 (MT3)-dependent developmental mechanism behind hindbrain vasculature development. We first demonstrate that MT3-regulates hindbrain vegfaa expression. We provide evidence that hindbrain neurons are not the source of vegfaa, instead, restricted pax6a+ neuroprogenitor cells (NPCs) instruct central arteries (CtAs) ingression into the hindbrain. Therefore, MT3 acts as an integrator, providing the regulatory cues necessary for the timely ingression of the CtAs into the hindbrain.
format Artículo científico
id pubmed_40593336
institution PubMed
language en
publishDate 2025
publisher Communications biology
record_format pubmed
spellingShingle Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafish.
Trindade, Marlene
Silva, Nádia
Rodrigues, Joana
Kawakami, Koichi
Campinho, Marco A
Animals
Zebrafish
Rhombencephalon
Zebrafish Proteins
Monocarboxylic Acid Transporters
Thyroid Hormones
Gene Expression Regulation, Developmental
Symporters
Female
Vascular Endothelial Growth Factor A
Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafish. Trindade, Marlene Silva, Nádia Rodrigues, Joana Kawakami, Koichi Campinho, Marco A Animals Zebrafish Rhombencephalon Zebrafish Proteins Monocarboxylic Acid Transporters Thyroid Hormones Gene Expression Regulation, Developmental Symporters Female Vascular Endothelial Growth Factor A Thyroid hormone (TH) signaling is important and necessary for proper neurodevelopment. Inadequate levels of maternally derived THs (MTH) supply affect target gene expression profiles, which are fundamental for the brain's normal growth, maturation, and function. The monocarboxylate transporter 8 (SLC16A2, MCT8) is the main TH transporter present in the brain during embryonic development, and mutations in this transporter lead to a rare and debilitating human condition known as the Allan-Herndon-Dudley Syndrome (AHDS). This mutation affects the capacity for intracellular transport of the hormone, leading to impaired brain development that constitutes the main pathophysiological basis of AHDS. Like humans, zebrafish embryos express slc16a2 that transports exclusively T3 at zebrafish physiological temperature. Studies in zebrafish Mct8 knockdown (KD) models found impaired hindbrain vasculature development. Here, using zebrafish Mct8 KD and knockout (KO) models, we shed light on the maternal T3 (MT3)-dependent developmental mechanism behind hindbrain vasculature development. We first demonstrate that MT3-regulates hindbrain vegfaa expression. We provide evidence that hindbrain neurons are not the source of vegfaa, instead, restricted pax6a+ neuroprogenitor cells (NPCs) instruct central arteries (CtAs) ingression into the hindbrain. Therefore, MT3 acts as an integrator, providing the regulatory cues necessary for the timely ingression of the CtAs into the hindbrain.
title Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafish.
topic Animals
Zebrafish
Rhombencephalon
Zebrafish Proteins
Monocarboxylic Acid Transporters
Thyroid Hormones
Gene Expression Regulation, Developmental
Symporters
Female
Vascular Endothelial Growth Factor A
url https://pubmed.ncbi.nlm.nih.gov/40593336/