Dynamic mRNA distribution pattern of thyroid hormone transporters and deiodinases during early embryonic chicken brain development

Geysens, Stijn; Ferrán, José Luis; Herck, Stijn L.J. Van; Tylzanowski, Przemko; Puelles, Luis; Darras, Veerle

doi:10.1016/j.neuroscience.2012.06.057

Cited by 36 publications

(25 citation statements)

References 64 publications

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“…High magnification imaging revealed EGFP expression in various cell types, including epithelial cells above the otic vesicle, in the olfactory bulb, and in the choroid plexus. This expression pattern is consistent with previous reports on chicken embryos (42,49) and mammals (43). The expression pattern in the choroid plexus suggests that MCT8 may play a role in the transport of THs into the cerebrospinal fluid.…”

Section: Discussionsupporting

confidence: 92%

“…Colocalization of EGFP and DsRed was also observed in vessels surrounding the brain; however, not in the region where zebrafish blood-brain barrier was identified (52). This finding is consistent with previous reports on chickens (42). In contrast, in rodents, MCT8 mRNA and protein were observed in the blood-brain barrier (53), suggesting that MCT8 is not directly involved in TH transport across the blood-brain barrier in non-mammalian vertebrates.…”

Section: Discussionsupporting

confidence: 88%

“…We found that mct8 was ubiquitously expressed at 10 hpf. As MCT8 transports THs, and maternal THs are important for early brain development (41,42), the observed mct8 expression implies that MCT8 may allow the accumulation of active THs, even at early developmental stages. At 1-2 dpf, mct8 was mainly expressed in the CNS, specifically in the forebrain, midbrain, hindbrain, and along the spinal cord and notochord.…”

Section: Discussionmentioning

confidence: 99%

“…Additional non-mammalian models, such as chicken and frog, were used to study the role of MCT8 in TH transport (2,42). However, although the role of MCT8 in regulating the TH endocrinological system is well characterized, the cause for the AHDS neurological symptoms and the mechanisms underlying MCT8 deficiency remain poorly understood.…”

Section: Discussionmentioning

confidence: 99%

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Zebrafish as a Model for Monocarboxyl Transporter 8-Deficiency

Vatine

Zada

Lerer-Goldshtein

et al. 2013

Journal of Biological Chemistry

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Background: Mutations in the thyroid hormone transporter MCT8 are associated with the psychomotor retardation Allan-Herndon-Dudley syndrome (AHDS). Results: In zebrafish, as in humans, mct8 is expressed primarily in the nervous system. Elimination of MCT8 causes severe neural impairment. Conclusion: MCT8 is a crucial regulator during zebrafish embryonic development. Significance: Establishment of the first vertebrate model for MCT8 deficiency, which exhibits a neurological phenotype.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Zebrafish as a Model for Monocarboxyl Transporter 8-Deficiency

Vatine

Zada

Lerer-Goldshtein

et al. 2013

Journal of Biological Chemistry

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“…In situ hybridisation (ISH) was performed on 12 µm cryosections using digoxigenin (DIG)-UTP-labelled antisense riboprobes as previously described (HidalgoSanchez et al 2005, Geysens et al 2012. Antisense and sense probes for chicken MCT8 and RORα were synthesised following the manufacturer's recommendations (Roche Diagnostics S.L., Applied Science).…”

Section: In Situ Hybridisationmentioning

confidence: 99%

MCT8 deficiency in Purkinje cells disrupts embryonic chicken cerebellar development

Delbaere

Vancamp

Herck

et al. 2017

Journal of Endocrinology

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Inactivating mutations in the human SLC16A2 gene encoding the thyroid hormone transporter monocarboxylate transporter 8 (MCT8) result in the Allan-Herndon-Dudley syndrome accompanied by severe locomotor deficits. The underlying mechanisms of the associated cerebellar maldevelopment were studied using the chicken as a model. Electroporation of an MCT8-RNAi vector into the cerebellar anlage of a 3-dayold embryo allowed knockdown of MCT8 in Purkinje cell precursors. This resulted in the downregulation of the thyroid hormone-responsive gene RORα and the Purkinje cell-specific differentiation marker LHX1/5 at day 6. MCT8 knockdown also results in a smaller and less complex dendritic tree at day 18 suggesting a pivotal role of MCT8 for cell-autonomous Purkinje cell maturation. Early administration of the thyroid hormone analogue 3,5,3′-triiodothyroacetic acid partially rescued early Purkinje cell differentiation. MCT8-deficient Purkinje cells also induced non-autonomous effects as they led to a reduced granule cell precursor proliferation, a thinner external germinal layer and a loss of PAX6 expression. By contrast, at day 18, the external germinal layer thickness was increased, with an increase in presence of Axonin-1-positive post-mitotic granule cells in the initial stage of radial migration. The concomitant accumulation of presumptive migrating granule cells in the molecular layer, suggests that inward radial migration to the internal granular layer is stalled. In conclusion, early MCT8 deficiency in Purkinje cells results in both cell-autonomous and non-autonomous effects on cerebellar development and indicates that MCT8 expression is essential from very early stages of development, providing a novel insight into the ontogenesis of the Allan-HerndonDudley syndrome.

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