Type I iodothyronine deiodinase in euthyroid and hypothyroid chicken cerebellum

Verhoelst, Carla; Darras, Veerle; Zandieh-Doulabi, Behrouz; Reyns, Geert; Kühn, Eduard; Geyten, Serge Van der

doi:10.1016/j.mce.2003.10.074

Cited by 25 publications

(16 citation statements)

References 40 publications

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“…In the normal E18 chicken cerebellum, the EGL has decreased significantly in thickness (Verhoelst et al 2004). After electroporation at E3, transfected PCs are found in a monolayer in the cerebellar folia and sagittal sections show a clearly defined PCL, ML and EGL.…”

Section: Mct8-rnai Transfection Of Pcs Results In a Retardation Of Gcmentioning

confidence: 95%

“…EGL thickness, proliferation and GC migration were affected downstream of MCT8 knockdown in PCs. Thus, although it is thought that GCs have an autonomous requirement for TH during their late maturation events, as shown by the delay in GC migration in hypothyroid rat and chicken (Verhoelst et al 2004, Shimokawa et al 2014, they are also indirectly dependent for normal development on TH signalling in PCs (Fig. 7).…”

Section: Mct8-deficient Pcs Disrupt Gc Precursor Proliferation and Pomentioning

confidence: 99%

“…Distinct cerebellar cell types depend on adequate TH levels as well as a correct timing of TH access to coordinate key cellular events driving the development and functional maintenance of the cerebellum (Koibuchi 2008, Faustino & Ortiga-Carvalho 2014. As such, induction of hypothyroidism in animal models such as rat and chicken 232:2 results in a number of morphological alterations, including impaired Purkinje cell (PC) dendritic arborisation, delayed granule cell (GC) migration from the external germinal layer (EGL) towards their final cortical position in the internal granular layer (IGL), delayed myelination and changes in synaptogenesis between cerebellar neurons and afferent neuronal fibres (Bouvet et al 1987, Verhoelst et al 2004, Anderson 2008, Shimokawa et al 2014. The role of 3,5,3′-triiodothyronine (T 3 ), the most active TH, in PC dendritogenesis has also been shown in vitro by the addition of T 3 to cerebellar cultures resulting in an increase in PC dendritic branching and calibre in a dose-and time-dependent manner (Heuer & Mason 2003).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Mct8-rnai Transfection Of Pcs Results In a Retardation Of Gcmentioning

confidence: 95%

Section: Mct8-deficient Pcs Disrupt Gc Precursor Proliferation and Pomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MCT8 deficiency in Purkinje cells disrupts embryonic chicken cerebellar development

Delbaere

Vancamp

Herck

et al. 2017

Journal of Endocrinology

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“…D1 mRNA has been detected in brain of several mammals, birds and fish, and even in Xenopus tadpoles (Bates et al 1999, Chan et al 2002, Morvan Dubois et al 2006, Johnson & Lema 2011, Van Herck et al 2012). This mRNA is translated at least in part into D1 protein as shown in chicken, where the amount of D1 protein in cerebellum was influenced by thyroid status (Verhoelst et al 2004). However, only minimal D1 activity could be found in brain tissue so far.…”

Section: Control Of Intracellular T 3 Availabilitymentioning

confidence: 87%

“…The few data available from birds (chicken) show some variation, but in most studies hyperthyroidism seemed to increase hepatic D1 activity, while hypothyroidism decreased hepatic D1 activity and also lowered D1 protein in brain (Decuypere et al 1987, Verhoelst et al 2004, Darras et al 2006. Data from fish studies show a different response of D1 to thyroid status.…”

Section: Response Of Deiodinases To Thyroid Statusmentioning

confidence: 99%

Iodothyronine deiodinase structure and function: from ascidians to humans

Darras

Herck

2012

Journal of Endocrinology

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Iodothyronine deiodinases are important mediators of thyroid hormone (TH) action. They are present in tissues throughout the body where they catalyse 3,5,3 0 -triiodothyronine (T 3 ) production and degradation via, respectively, outer and inner ring deiodination. Three different types of iodothyronine deiodinases (D1, D2 and D3) have been identified in vertebrates from fish to mammals. They share several common characteristics, including a selenocysteine residue in their catalytic centre, but show also some type-specific differences. These specific characteristics seem very well conserved for D2 and D3, while D1 shows more evolutionary diversity related to its Km, 6-n-propyl-2-thiouracil sensitivity and dependence on dithiothreitol as a cofactor in vitro. The three deiodinase types have an impact on systemic T 3 levels and they all contribute directly or indirectly to intracellular T 3 availability in different tissues. The relative contribution of each of them, however, varies amongst species, developmental stages and tissues. This is especially true for amphibians, where the impact of D1 may be minimal. D2 and D3 expression and activity respond to thyroid status in an opposite and conserved way, while the response of D1 is variable, especially in fish. Recently, a number of deiodinases have been cloned from lower chordates. Both urochordates and cephalochordates possess selenodeiodinases, although they cannot be classified in one of the three vertebrate types. In addition, the cephalochordate amphioxus also expresses a non-selenodeiodinase. Finally, deiodinase-like sequences have been identified in the genome of non-deuterostome organisms, suggesting that deiodination of externally derived THs may even be functionally relevant in a wide variety of invertebrates.

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Spatial and temporal expression profiles of urocortin 3 mRNA in the brain of the chicken (Gallus gallus)

Grommen

Scott

Darras

et al. 2017

J of Comparative Neurology

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Urocortin 3 (UCN3) is a neuropeptide believed to regulate stress-coping responses by binding to type 2 corticotropin-releasing hormone receptors. Here, we report the cloning and brain distribution of UCN3 mRNA in a sauropsid-the chicken, Gallus gallus. Mature chicken UCN3 is predicted to be a 40-amino acid peptide showing high sequence similarity to human (93%), mouse (93%), and Xenopus (88%) UCN3. During the last third of embryonic development, UCN3 mRNA levels changed differentially in the various brain parts. In all brain parts, UCN3 mRNA levels tended to increase toward hatching, except for caudal brainstem, where a gradual decrease was observed during the last week of embryonic development. In cerebellum, a rapid increase in gene expression occurred between embryonic days 17 and 19. Using in situ hybridization, UCN3 mRNA was found to be expressed predominantly in the hypothalamus, pons, and medulla of posthatch chick brains, but not in some areas that are among the main expression sites in rodents, such as the brain areas where in mammals the median preoptic nucleus and the medial amygdala are located. This suggests that the roles of UCN3 in chicken, and perhaps sauropsids in general, are not all identical to those in rodents.

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Type I iodothyronine deiodinase in euthyroid and hypothyroid chicken cerebellum

Cited by 25 publications

References 40 publications

MCT8 deficiency in Purkinje cells disrupts embryonic chicken cerebellar development

MCT8 deficiency in Purkinje cells disrupts embryonic chicken cerebellar development

Iodothyronine deiodinase structure and function: from ascidians to humans

Spatial and temporal expression profiles of urocortin 3 mRNA in the brain of the chicken (Gallus gallus)

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