Main Factors Involved in Thyroid Hormone Action

Tedeschi, Lorena; Vassalle, Cristina; Iervasi, Giorgio; Sabatino, Laura

doi:10.3390/molecules26237337

Cited by 11 publications

(9 citation statements)

References 64 publications

(74 reference statements)

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“…The main mechanism of TH action is the modulation of gene expression by the binding of the nuclear active hormone T3 to specific nuclear receptors, although indirect genomic actions by both T3 and T4 have also been described by their binding to different receptors at the cytoplasmic membrane, cytoplasm and mitochondria [ 4 , 5 ]. TH action in the brain is a complex process that allows the spatiotemporal regulation of the expression of genes involved in many developmental and physiological processes such as neural cell proliferation and differentiation, neuronal migration, and cortical lamination [ 3 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Thyroid Hormone Transporters MCT8 and OATP1C1 Are Expressed in Pyramidal Neurons and Interneurons in the Adult Motor Cortex of Human and Macaque Brain

Wang

Montero-Pedrazuela

et al. 2023

IJMS

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Monocarboxylate transporter 8 (MCT8) and organic anion transporter polypeptide 1C1 (OATP1C1) are thyroid hormone (TH) transmembrane transporters that play an important role in the availability of TH for neural cells, allowing their proper development and function. It is important to define which cortical cellular subpopulations express those transporters to explain why MCT8 and OATP1C1 deficiency in humans leads to dramatic alterations in the motor system. By means of immunohistochemistry and double/multiple labeling immunofluorescence in adult human and monkey motor cortices, we demonstrate the presence of both transporters in long-projection pyramidal neurons and in several types of short-projection GABAergic interneurons in both species, suggesting a critical position of these transporters for modulating the efferent motor system. MCT8 is present at the neurovascular unit, but OATP1C1 is only present in some of the large vessels. Both transporters are expressed in astrocytes. OATP1C1 was unexpectedly found, only in the human motor cortex, inside the Corpora amylacea complexes, aggregates linked to substance evacuation towards the subpial system. On the basis of our findings, we propose an etiopathogenic model that emphasizes these transporters’ role in controlling excitatory/inhibitory motor cortex circuits in order to understand some of the severe motor disturbances observed in TH transporter deficiency syndromes.

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Section: Introductionmentioning

confidence: 99%

Thyroid Hormone Transporters MCT8 and OATP1C1 Are Expressed in Pyramidal Neurons and Interneurons in the Adult Motor Cortex of Human and Macaque Brain

Wang

Montero-Pedrazuela

et al. 2023

IJMS

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“…( 66 ). Thyroid hormones can also act through binding sites at plasma membrane such as integrin αvβ3 ( 67 ).…”

Section: Thyroid Hormone Physiologymentioning

confidence: 99%

Inherited Disorders of Thyroid Hormone Metabolism Defect Caused by the Dysregulation of Selenoprotein Expression

et al. 2022

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Consistent activation and functioning of thyroid hormones are essential to the human body as a whole, especially in controlling the metabolic rate of all organs and systems. Impaired sensitivity to thyroid hormones describes any process that interferes with the effectiveness of thyroid hormones. The genetic origin of inherited thyroid hormone defects and the investigation of genetic defects upon the processing of thyroid hormones are of utmost importance. Impaired sensitivity to thyroid hormone can be categorized into three conditions: thyroid hormone cell membrane transport defect (THCMTD), thyroid hormone metabolism defect (THMD), and thyroid hormone action defect (THAD). THMD is caused by defects in the synthesis and processing of deiodinases that convert the prohormone thyroxine (T4) to the active hormone triiodothyronine (T3). Deiodinase, a selenoprotein, requires unique translation machinery that is collectively composed of the selenocysteine (Sec) insertion sequence (SECIS) elements, Sec-insertion sequence-binding protein 2 (SECISBP2), Sec-specific eukaryotic elongation factor (EEFSEC), and Sec-specific tRNA (TRU-TCA1-1), which leads to the recognition of the UGA codon as a Sec codon for translation into the growing polypeptide. In addition, THMD could be expanded to the defects of enzymes that are involved in thyroid hormone conjugation, such as glucuronidation and sulphation. Paucity of inherited disorders in this category leaves them beyond the scope of this review. This review attempts to specifically explore the genomic causes and effects that result in a significant deficiency of T3 hormones due to inadequate function of deiodinases. Moreover, along with SECISBP2, TRU-TCA1-1, and deiodinase type-1 (DIO1) mutations, this review describes the variants in DIO2 single nucleotide polymorphism (SNP) and thyroid stimulating hormone receptor (TSHR) that result in the reduced activity of DIO2 and subsequent abnormal conversion of T3 from T4. Finally, this review provides additional insight into the general functionality of selenium supplementation and T3/T4 combination treatment in patients with hypothyroidism, suggesting the steps that need to be taken in the future.

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“…Cell proliferation, angiogenesis, microfilament organization, and thermogenesis are all affected and regulated by this activity. Nongenomic and genomic functions, on the other hand, influence and overlap each other to control cellular metabolism and development 6–8 …”

Section: Introductionmentioning

confidence: 99%

“…Nongenomic and genomic functions, on the other hand, influence and overlap each other to control cellular metabolism and development. 6 , 7 , 8 …”

Section: Introductionmentioning

confidence: 99%

“…Nongenomic and genomic functions, on the other hand, influence and overlap each other to control cellular metabolism and development. [6][7][8] Altman et al showed the presence of alpha and beta THR in human larynx especially in the fibrous connective tissue of the lamina propria of the vocal cords. 9 Despite hypothyroidism's impact on the larynx, the pathophysiology of voice problems in hypothyroidism remains a controversial issue.…”

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confidence: 99%

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Histopathological characteristics of larynx in hypothyroidism in an experimental rabbit model

Iravani

Golkhar

Azarpira

et al. 2022

Laryngoscope Investig Oto

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Objective Hypothyroidism has a significant effect on the patients' voices. This study evaluated the histopathological characteristics of larynx following hypothyroidism in an experimental rabbit model. Methods Eleven male Dutch rabbits were included. Methimazole‐induced hypothyroidism was done for nine rabbits. The remaining two rabbits were assigned as controls. Six weeks after starting methimazole, a histological examination was performed with parameters of inflammation, ulceration, hemorrhage, and thickness of epithelium, Reinke's space, vocal ligament, thyroarytenoid muscle, collagen deposition, and periodic acid‐Schiff (PAS)‐positive materials, as well as confirmation of hypothyroidism by T4 measurement. Results Histologic examination showed a significant thickening of epithelium, Reinke's space, vocal ligament, and collagen PAS‐positive materials deposition in hypothyroid rabbits (p < .05). There was significant reduction in thyroarytenid muscle thickness (p < .05). Inflammation, ulceration, and bleeding were not significantly different between hypothyroid and control rabbits' laryngeal specimens. Conclusion Hypothyroidism causes significant changes in the laryngeal tissues. Thickening of epithelium, Reinke's space, vocal ligament, collagen, PAS‐positive materials, and reduced thickness of thyroarytenoid muscle are the major findings of this study.

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Main Factors Involved in Thyroid Hormone Action

Cited by 11 publications

References 64 publications

Thyroid Hormone Transporters MCT8 and OATP1C1 Are Expressed in Pyramidal Neurons and Interneurons in the Adult Motor Cortex of Human and Macaque Brain

Thyroid Hormone Transporters MCT8 and OATP1C1 Are Expressed in Pyramidal Neurons and Interneurons in the Adult Motor Cortex of Human and Macaque Brain

Inherited Disorders of Thyroid Hormone Metabolism Defect Caused by the Dysregulation of Selenoprotein Expression

Histopathological characteristics of larynx in hypothyroidism in an experimental rabbit model

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