Functional TSH Receptors, Malignant Melanomas and Subclinical Hypothyroidism

Ursu, H

doi:10.1159/000339817

Cited by 4 publications

(7 citation statements)

References 3 publications

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“…( 169 ); Figures 3 J,K]. Recently, the hippocampus of developmentally hypothyroid pups showed altered VGluT1/VGAT immunoreactivity ( 180 ). Although Camk4/Creb pathway plays a fundamental role in neurites growth and establishment of synapses, other genes are involved in the development of hippocampal connections.…”

Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

“…In agreement, GAP-43 −/− mice failed to express 5-HTT in the barrel cortex causing a disrupted segregation of thalamic afferents in the barrel cortex. In addition, recent data show that the density of VGluT1-immunoreactive buttons is decreased in layer IV of the parietal cortex of hypothyroid rats ( 180 ). These data show that there is an asynchrony in the maturation of thalamocortical afferents and their cortical targets in hypothyroid rats.…”

Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

“…On the other hand, Camk4 regulates the transcriptional activity of the TR, which might be due to direct phosphorylation of co-activators or by changing the equilibrium between the co-activators and the silencing mediator for retinoid and thyroid hormone receptors (SMRT) ( 178 , 179 ). Camk4/Creb pathway and downstream targets are involved in processes such as neurogenesis, biosynthesis, and assembly of cytoskeleton, cell movement and migration, neurite development and maturation, synaptic plasticity, and neurotransmission ( 44 , 180 ). In humans, Camk4/Creb pathway is involved in psychiatric disorders ( 181 – 183 ).…”

Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

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An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

2014

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The morphological alterations of cortical lamination observed in mouse models of developmental hypothyroidism prompted the recognition that these experimental changes resembled the brain lesions of children with autism; this led to recent studies showing that maternal thyroid hormone deficiency increases fourfold the risk of autism spectrum disorders (ASD), offering for the first time the possibility of prevention of some forms of ASD. For ethical reasons, the role of thyroid hormones on brain development is currently studied using animal models, usually mice and rats. Although mammals have in common many basic developmental principles regulating brain development, as well as fundamental basic mechanisms that are controlled by similar metabolic pathway activated genes, there are also important differences. For instance, the rodent cerebral cortex is basically a primary cortex, whereas the primary sensory areas in humans account for a very small surface in the cerebral cortex when compared to the associative and frontal areas that are more extensive. Associative and frontal areas in humans are involved in many neurological disorders, including ASD, attention deficit-hyperactive disorder, and dyslexia, among others. Therefore, an evo-devo approach to neocortical evolution among species is fundamental to understand not only the role of thyroid hormones and environmental thyroid disruptors on evolution, development, and organization of the cerebral cortex in mammals but also their role in neurological diseases associated to thyroid dysfunction.

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Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

See 1 more Smart Citation

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

2014

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“…Shortly thereafter, the same group found that melanocyte-originated lesions ranging from a benign nevus, dysplastic nevi, and melanoma all express functional TSHR, with an upregulated expression in premalignant and malignant lesions, implying a higher sensitivity to TSH [48]. Combining this with the study that found TSH can promote the growth of melanoma by triggering the formation of cAMP and activating the mitogen-activated protein kinase (MAPK) signaling pathway, may in part account for the high prevalence of hypothyroidism (elevated TSH lever) in the melanoma population [48,49]. Intriguingly, another study has reported that suppression of MAP kinase and PI3KAkt pathways exhibits their anti-melanoma effects, including suppression of cell proliferation, transformation, and invasion, and these effects are coupled with inducing the expression of thyroid genes, such as TSH-R and NIS, and consequently increasing radioiodide uptake by melanoma cells, which may prove to be a novel approach to treating melanoma [50,51].…”

Section: Hypothalamic-pituitary-thyroid Axis (Hpt) Homologmentioning

confidence: 95%

Recognition of Melanocytes in Immuno-Neuroendocrinology and Circadian Rhythms: Beyond the Conventional Melanin Synthesis

Chen

Liu

Zhou

et al. 2022

Cells

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Melanocytes produce melanin to protect the skin from UV-B radiation. Notwithstanding, the spectrum of their functions extends far beyond their well-known role as melanin production factories. Melanocytes have been considered as sensory and computational cells. The neurotransmitters, neuropeptides, and other hormones produced by melanocytes make them part of the skin’s well-orchestrated and complex neuroendocrine network, counteracting environmental stressors. Melanocytes can also actively mediate the epidermal immune response. Melanocytes are equipped with ectopic sensory systems similar to the eye and nose and can sense light and odor. The ubiquitous inner circadian rhythm controls the body’s basic physiological processes. Light not only affects skin photoaging, but also regulates inner circadian rhythms and communicates with the local neuroendocrine system. Do melanocytes “see” light and play a unique role in photoentrainment of the local circadian clock system? Why, then, are melanocytes responsible for so many mysterious functions? Do these complex functional devices work to maintain homeostasis locally and throughout the body? In addition, melanocytes have also been shown to be localized in internal sites such as the inner ear, brain, and heart, locations not stimulated by sunlight. Thus, what can the observation of extracutaneous melanocytes tell us about the “secret identity” of melanocytes? While the answers to some of these intriguing questions remain to be discovered, here we summarize and weave a thread around available data to explore the established and potential roles of melanocytes in the biological communication of skin and systemic homeostasis, and elaborate on important open issues and propose ways forward.

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“…Indeed, TSH has been recognized as a tumor promoting factor not only for DTC, but even for other ETM such as ovarian cancer and hepatocellular carcinoma [ 106 ]. TSH receptor (TSHR) expression, at both mRNA and protein level, has been documented in skin tissues and different skin cell types including cultured keratinocytes, dermal fibroblasts, epidermal melanocytes, and melanoma cells [ 102 , 107 , 108 , 109 , 110 ]. In particular, Ellerhorst and colleagues detected the TSHR in all cutaneous melanocytic lesions, namely benign nevi, dysplastic nevi, and melanomas [ 109 ].…”

Section: Hormonal Players Of the Hypothalamic–pituitary–thyroid Axis ...mentioning

confidence: 99%

Is Melanoma Progression Affected by Thyroid Diseases?

Ulisse

Baldini

Pironi

et al. 2022

IJMS

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Clinical and epidemiological evidence indicate a relationship between thyroid diseases and melanoma. In particular, the hypothyroidism condition appears to promote melanoma spread, which suggests a protective role of thyroid hormones against disease progression. In addition, experimental data suggest that, in addition to thyroid hormones, other hormonal players of the hypothalamic–pituitary–thyroid (HPT) axis, namely the thyrotropin releasing hormone and the thyrotropin, are likely to affect melanoma cells behavior. This information warrants further clinical and experimental studies in order to build a precise pattern of action of the HPT hormones on melanoma cells. An improved knowledge of the involved molecular mechanism(s) could lead to a better and possibly personalized clinical management of these patients.

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Functional TSH Receptors, Malignant Melanomas and Subclinical Hypothyroidism

Cited by 4 publications

References 3 publications

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

Recognition of Melanocytes in Immuno-Neuroendocrinology and Circadian Rhythms: Beyond the Conventional Melanin Synthesis

Is Melanoma Progression Affected by Thyroid Diseases?

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