Effects of neonatal hypothyroidism on the expressions of growth cone proteins and axon guidance molecules related genes in the hippocampus

Wong, Chun–Ming; Leung, Mun-Fai

doi:10.1016/s0303-7207(01)00592-5

Cited by 24 publications

(17 citation statements)

References 33 publications

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“…During normal development, neural migration and maturation of neural and glial cells are guided by TH (Alvarez-Dolado et al 1999; Wong and Leung 2001). Therefore, hypothyroidism during development causes a large number of neuroanatomical and behavioral effects (Haddow et al 1999; Schalock et al 1977; Zoeller and Crofton 2005).…”

Section: Discussionmentioning

confidence: 99%

Polybrominated Diphenyl Ethers Induce Developmental Neurotoxicity in a Human in Vitro Model: Evidence for Endocrine Disruption

Schreiber

Gaßmann

Götz

et al. 2010

Environ Health Perspect

190

139

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BackgroundPolybrominated diphenyl ethers (PBDEs) are persistent and bioaccumulative flame retardants, which are found in rising concentrations in human tissues. They are of concern for human health because animal studies have shown that they possess the potential to be developmentally neurotoxic.ObjectiveBecause there is little knowledge of the effects of PBDEs on human brain cells, we investigated their toxic potential for human neural development in vitro. Moreover, we studied the involvement of thyroid hormone (TH) disruption in the effects caused by PBDEs.MethodsWe used the two PBDE congeners BDE-47 and BDE-99 (0.1–10 μM), which are most prominent in human tissues. As a model of neural development, we employed primary fetal human neural progenitor cells (hNPCs), which are cultured as neurospheres and mimic basic processes of brain development in vitro: proliferation, migration, and differentiation.ResultsPBDEs do not disturb hNPC proliferation but decrease migration distance of hNPCs. Moreover, they cause a reduction of differentiation into neurons and oligodendrocytes. Simultaneous exposure with the TH receptor (THR) agonist triiodothyronine rescues these effects on migration and differentiation, whereas the THR antagonist NH-3 does not exert an additive effect.ConclusionPBDEs disturb development of hNPCs in vitro via endocrine disruption of cellular TH signaling at concentrations that might be of relevance for human exposure.

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Section: Discussionmentioning

confidence: 99%

Polybrominated Diphenyl Ethers Induce Developmental Neurotoxicity in a Human in Vitro Model: Evidence for Endocrine Disruption

Schreiber

Gaßmann

Götz

et al. 2010

Environ Health Perspect

190

139

View full text Add to dashboard Cite

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“…Interestingly, BDNF was also found involved in the activation of Erk1/2 signaling pathway (188), which affects not only the differentiation of hippocampal neurons but also almost all aspects of corticogenesis (Tables 3–6). However, the inactivation of other pathways such as the Gsk3β/CRMP2 pathway will result in delayed axonal growth (251, 257). Decreased p-Gsk3β labeling and increased labeling of its inactivated p-CRMP2 target protein was seen in the developmentally hypothyroid and hypothyroxinemic rat hippocampus (251).…”

Section: Alterations In Cortical Development Caused By Thyroid Hormonmentioning

confidence: 99%

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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“…The use of some of the above-cited genes as internal controls for ribonucleic acid (RNA) quantification in the brain has been recently questioned, as their expression is modulated under different physiological and pathological circumstances, both in vivo and in vitro. For example, recent researches have demonstrated that sex differences and the secretion of hormones and neurotrophins could be sources of variability for Gapdh and Actb (Matsumoto et al 1994; Barroso et al 1999;Perrot-Sinal et al 2001;Wong and Leung 2001;Zhang et al 2001). In addition, it has been observed that Gapdh transcript and protein were upregulated in neuronal apoptosis (Sawa et al 1997;Ishitani et al 1998;Chen et al 1999;Yang et al 2007), which is an important mechanism for brain development, homeostasis, and disease.…”

Section: Introductionmentioning

confidence: 99%

Selection of Reference Genes for Quantitative Real-time RT-PCR Studies in Mouse Brain

et al. 2008

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Since a growing number of studies based on the real-time reverse transcriptase polymerase chain reaction (RT-PCR) continue to be published in order to highlight genes specifically involved in brain development, maturation, and function, the identification of reference genes suitable for this kind of experiments is now an urgent need in the neuroscience field. The aim of this work was to verify the suitability of some very common housekeeping genes (such as Gapdh, 18s, and B2m) and of some relatively new control genes (such as Pgk1, Tfrc, and Gusb) during mouse brain maturation. We tested the candidate reference genes in mouse whole brain, cerebellum, brain stem, hippocampus, medial septum, frontal neocortex, and olfactory bulb. Moreover, we reported the first complete study of Pgk1 expression throughout the development and the aging of mouse brain. Although no tested gene showed to be the optimal reference for all mouse brain regions, in general, the new housekeeping genes were highly stable in most of the analyzed regions. Above all, with few exceptions, Pgk1 showed to be a reliable control for the analyzed mouse brain regions during development, maturation, and aging.

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Effects of neonatal hypothyroidism on the expressions of growth cone proteins and axon guidance molecules related genes in the hippocampus

Cited by 24 publications

References 33 publications

Polybrominated Diphenyl Ethers Induce Developmental Neurotoxicity in a Human in Vitro Model: Evidence for Endocrine Disruption

Polybrominated Diphenyl Ethers Induce Developmental Neurotoxicity in a Human in Vitro Model: Evidence for Endocrine Disruption

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

Selection of Reference Genes for Quantitative Real-time RT-PCR Studies in Mouse Brain

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