Thyroid Development and Effect on the Nervous System

Santisteban, Pilar; Bernal, Juan

doi:10.1007/s11154-005-3053-9

Cited by 77 publications

(66 citation statements)

References 66 publications

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“…In a few contexts, such as that of Pax8 in the thyroid, these proteins have been characterized as essential for tissue maintenance. 15 However, most cells tend to downregulate the expression of Pax proteins following organogenesis. Persistent expression of these proteins may have a deleterious effect under many circumstances.…”

Section: Discussionmentioning

confidence: 99%

PAX3 expression in primary melanomas and nevi

et al. 2008

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Melanoma is responsible for an estimated 62 000 new American cancer diagnoses and is projected to cause nearly 8000 deaths in 2008 alone. Although the histogenesis of the tumor is not well understood, it is thought to originate from a rare melanocyte stem cell that resides in the skin. The transcription factor PAX3 has a wellestablished role in the development of melanocytes during embryogenesis, and has recently been characterized as a molecular switch in the mature melanocyte. Based on this function, PAX3 promotes a melanocytic phenotype but blocks terminal differentiation. This mechanism may also contribute to the uncontrolled cell growth and loss of terminal differentiation in melanomas. Here, we find PAX3 expression in 8/8 melanoma cell lines. We also find that PAX3 is commonly expressed in primary melanoma samples (21/58) but significantly less frequently in benign pigmented lesions (9/75). Further analysis of our melanoma set revealed that PAX3 expression is strongly correlated with younger patients with low or no evidence of sun damage. Our data suggest that PAX3-expressing melanomas may be less environmentally dependent and more genetically linked.

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Section: Discussionmentioning

confidence: 99%

PAX3 expression in primary melanomas and nevi

et al. 2008

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“…myelin basic protein, proteolipid protein, myelin associated glycoprotein) and neuronal differentiation (i.e. nerve growth factor (NGF), brainderived neurotropic factor (BDNF); König & Neto 2002, Santisteban & Bernal 2005. Accordingly, it has been shown that early maternal hypothyroxinemia alters fetal brain histogenesis and cytoarchitecture in rats (Lavado-Autric et al 2003), and unrecognized hypothyroidism in women in the first trimester of pregnancy may adversely affect the neuropsychological development of the progeny (Haddow et al 1999, Pop et al 2003, Morreale de Escobar et al 2004.…”

Section: Seladin-1 As a Mediator Of The Effects Of Thyroid Hormones (mentioning

confidence: 99%

Neuroprotective effects of the Alzheimer's disease-related gene seladin-1

Peri

Serio

2008

Journal of Molecular Endocrinology

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The endocrine and the nervous system are closely correlated throughout life, starting from the embryo and until the late stages of life. Alzheimer's disease (AD) is the most common neurodegenerative disease associated with ageing. Unfortunately, an effective way to prevent or to cure this disease does not exist, so far. There is evidence that estrogens exert neuroprotective properties, although their efficacy against AD is still a matter of debate. In 2000 a new neuroprotective gene, i.e. seladin-1 (for SELective AD INdicator-1) was identified and found to be down regulated in AD vulnerable brain regions. Seladin-1 inhibits the activation of caspase-3, a key modulator of apoptosis. This protein has also enzymatic activity. In fact, it has been demonstrated that the seladin-1 gene encodes 3-b-hydroxysterol D-24-reductase, which catalyzes the synthesis of cholesterol from desmosterol. In recent years, it has been demonstrated that an appropriate amount of membrane cholesterol determines the generation of a barrier against toxic insults and prevents the production of b-amyloid, the histopathological hallmark of AD. This review will summarize the studies that have been focused on the characterization of the biological properties of seladin-1 since its first identification. In particular, the relationship between seladin-1-mediated neuroprotection and estrogens, IGF1 and thyroid hormones, will be described and discussed.

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“…In the rat THs deficiency during the suckling period results in marked retardation of brain growth and development (for reviews of earlier literature see Dussault & Ruel, 1987;Lauder, 1983;Paternostro & Meisami, 1993;Timiras, 1988; for reviews of more recent literature see Bernal, 2002;Morreale de Escobar et al, 2004;Santisteban & Bernal, 2005;Smith et al, 2002. Early studies on the effects of thyroid deficiency on brain development focused on structural abnormalities in the cerebral cortex (Eayrs, 1955(Eayrs, ,1966Rabie et al, 1979) and cerebellum (Lauder, 1983;Legrand et al, 1986, Patel & Rabie, 1980.…”

Section: Introductionmentioning

confidence: 99%

Novel two-dimensional morphometric maps and quantitative analysis reveal marked growth and structural recovery of the rat hippocampal regions from early hypothyroid retardation

Farahvar

Meisami

2007

Experimental Neurology

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Effects of postnatal hypothyroidism and recovery from this condition on regional growth of the rat hippocampus (HC) were studied using two-dimensional (2D) foldout, morphometric maps of HC and its constituent CA1-CA4 regions. The maps were derived from unfolding serial coronal sections of the rat forebrain, consisting of the entire rostrocaudal extent of HC pyramidal cell layer in the normal control and hypothyroid weanling (P25, postnatal day 25) and young adult (P90) male rats, as well as animals allowed to recover from hypothyroid-induced growth retardation at weaning. The maps revealed novel views of HC regions for assessment of topological relationships and measurement of surface areas of the HC cortical sheet (pyramidal cell layer). In normal control P90 rats, the unfolded HC on each side extended 4 times more laterally than rostrocaudally; total HC surface area was about 40 mm 2 , compared to 30 mm 2 in the weanling, indicating 35% growth from P25 to P90; CA1 took up 52% of the total HC surface area, followed by CA3 (31%) and CA2 and CA4, 8% each. Hypothyroidism resulted in significant (p<0.01) 11% and 20% reductions in the HC surface area in P25 and P90 rats respectively; CA1 and CA4 regions suffered the most reductions while CA3 and CA2 regions the least. Recovering rats examined at P90, exhibited remarkable growth plasticity and recovery in HC regions, as evident by their near normal HC cortical surface area values, compared to age-matched controls. The 2-D maps also revealed growth deficits in all HC regions of the hypothyroid rats; recovery in these parameters occurred across all dimensions, although the anterior-posterior growth was more severely affected than the mediolateral one. These results are confirmed and extended by volumetric analysis of laminar volumes of HC regions presented in a companion paper (Farahvar et al., 2006). These results imply that HC regions, in contrast to whole brain, possess exceptional growth plasticity, as shown by ability to dramatically recover from early hypothyroid retardation; also 2D morphometric maps are useful tools to visualize complex and convoluted regional sheet of HC cortex and depict quantitative aspects of growth in normal and experimental conditions.

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Thyroid Development and Effect on the Nervous System

Cited by 77 publications

References 66 publications

PAX3 expression in primary melanomas and nevi

PAX3 expression in primary melanomas and nevi

Neuroprotective effects of the Alzheimer's disease-related gene seladin-1

Novel two-dimensional morphometric maps and quantitative analysis reveal marked growth and structural recovery of the rat hippocampal regions from early hypothyroid retardation

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