Regulation of the L1 Cell Adhesion Molecule by Thyroid Hormone in the Developing Brain

Álvarez‐Dolado, Manuel; Cuadrado, Ana; Navarro-Yubero, Cristina; Sonderegger, P.; Furley, Andrew J.; Bernal, Juan; Múñoz, Alberto

doi:10.1006/mcne.2000.0879

Cited by 52 publications

(29 citation statements)

References 74 publications

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“…It is not known whether the cells that produce this protein, the Cajal-Retzius cells, contain thyroid hormone receptors, but they express another thyroid hormone-regulated gene, prostaglandin D2 synthase, which has thyroid responsive elements and may thus be a direct target of thyroid hormone [57]. Other molecules reported to be involved in cell migration, such as laminin, tenascin C, and LI, are also under thyroid hormone control [58,59].…”

Section: Nuclear Receptorsmentioning

confidence: 94%

Thyroid Development and Effect on the Nervous System

Santisteban

Bernal

2005

Rev Endocr Metab Disord

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Section: Nuclear Receptorsmentioning

confidence: 94%

Thyroid Development and Effect on the Nervous System

Santisteban

Bernal

2005

Rev Endocr Metab Disord

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“…In a study by another research group, western blot analysis of cerebellar extracts of postnatal rat pups following prenatal exposure to the same PCB mixture was found to decrease the expression of the neural cell adhesion molecule L1, which is under positive TH control (85,86). In contrast, it increased glial fibrillary acidic protein (GFAP) expression (86).…”

Section: Neurodevelopmental Effects Of Pcbsmentioning

confidence: 97%

Endocrine disrupting polyhalogenated organic pollutants interfere with thyroid hormone signalling in the developing brain

Darras¹

2008

Cerebellum

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Persistent polyhalogenated organic pollutants are present worldwide and accumulate along the food chain. They interfere with human and animal health and are particularly harmful for pre- and perinatal neurodevelopment. The mechanisms behind the observed effects vary depending on the specific compound investigated. Co-planar polychlorinated biphenyls (PCBs) can act via the arylhydrocarbon receptor while many ortho-substituted PCBs disrupt intracellular Ca(2+) homeostasis. A common mechanism for a wide variety of PCBs is interference with thyroid hormone (TH) signalling in developing brain, by changing intracellular TH availability or by interacting directly at the level of the TH receptors. Studies on gene expression in cortex and cerebellum revealed both hypothyroid- and hyperthyroid-like effects. However, since THdependent gene expression plays a crucial role in the coordination of neuronal proliferation, migration, synaptogenesis, myelination, etc., both reduced/delayed and increased/premature expression may result in permanent structural changes in neuronal communication networks, leading to lifelong deficits in cognitive performance, motor functions, and psychobehavior. In a similar way, PCBs are able to interfere with estrogen- and androgen-dependent brain development and in some studies neurobehavioral outcome was shown to be gender-specific. Other persistent organohalogens like polychlorinated dibenzo-p-dioxins (PCDDs) and polybrominated diphenyl ethers (PBDEs) also act as endocrine disrupters in the developing brain. Several of the mechanisms involved are similar to those of PCBs, but each group also works via own specific pathways. The fact that persistent organohalogens can amplify the neurotoxic effects of other environmental pollutants, such as heavy metals, further increases their risk for human and animal neurodevelopment.

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“…Remarkably, the expression of Reelin, a secreted extracellular matrix protein that has an important role in the control of neuronal migration and connectivity in the cerebral neocortex, is regulated by T 3 /T 4 during the perinatal period in the rat [41]. Moreover, we have previously described that at least two members of the immunoglobulin family of cell adhesion molecules expressed by neural cells such as L1 and TAG-1/axonin that modulate cellto-cell and cell-to-matrix interactions during development are also controlled by the thyroid in the CNS [42,43]. Whether or not the described anomalies may be reversible at advanced postnatal stages of development and whether they can be relieved or ameliorated by T 3 /T 4 administration constitute pivotal questions that are currently under investigation.…”

Section: Discussionmentioning

confidence: 99%

Low Thyroid Hormone Levels Impair the Perinatal Development of the Rat Retina

Sevilla-Romero¹,

Múñoz

Pinazo-Durán

2002

Ophthalmic Res

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Eye development is regulated by multiple agents including hormones and growth factors. Thyroid hormone (triiodothyronine, or T₃, and the prohormone thyroxine, or T₄) plays a crucial role in the development of the central nervous system. Here we have examined the effects of low T₃/T₄ levels (hypothyroid status) on the developing rat retina during the perinatal stage. Eyes from control (CG) and T₃/T₄-deficient (HG) fetuses (E19 and E21) and newborn (P0, P3, P5 and P7) rats were obtained by administering a chemical antithyroid solution (0.02% methyl-mercaptoimidazole +1% ClOK₄) in the tap water to the dams and their offspring, from E9 and throughout gestation until they were killed. Perinatal eyes were processed for light and electron transmission microscopy and subjected to morphological and morphometric analyses. Low T₃/T₄ levels led to decreased retinal growth during the perinatal stage. In addition, the retinas from the HG presented fewer neuroblasts than those of their euthyroid counterparts (at E21: 705 ± 83 cells per constant area of 4 × 10⁴ µm² vs. 440 ± 60 cells per constant area of 4 × 10⁴ µm²; p = 0.010). During development the index of mitosis in the retina peaked at E21, falling at the end of the 1st postnatal week. Significantly lower values were observed in the HG (at P5: 0.803 ± 0.374 mitoses/cells % vs. 0.349 ± 0.180 mitoses/cells %; p = 0.004). Furthermore, we have found that low T₃/T₄ levels delayed and/or altered a series of developmental processes occurring in the retina during the perinatal stage such as layering and differentiation of several cell types. Our results demonstrate that thyroid hormone regulates rat neuroretinogenesis.

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Regulation of the L1 Cell Adhesion Molecule by Thyroid Hormone in the Developing Brain

Cited by 52 publications

References 74 publications

Thyroid Development and Effect on the Nervous System

Thyroid Development and Effect on the Nervous System

Endocrine disrupting polyhalogenated organic pollutants interfere with thyroid hormone signalling in the developing brain

Low Thyroid Hormone Levels Impair the Perinatal Development of the Rat Retina

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