Treatment with Iodine in Pregnant Rats with Marginal Iodine Deficiency Improves Cell Migration in the Developing Brain of the Progeny

Zhang, Le; Zhai, Xiaodan; Liu, Yuhui; Li, Jing; Shan, Zhongyan; Wang, Teng

doi:10.1007/s12035-015-9155-9

Cited by 8 publications

(3 citation statements)

References 34 publications

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“…Hypothyroidism reduces reelin expression during neurodevelopment in early stages of noxa [29]. The effect of the administration of exogenous thyroid hormones on reelin levels in rodents has been studied [30]. In our series, hypothyroidism was analyzed separately from the reelin variable due to published evidence, but there was only one case of hypothyroidism in the analyzed sample, and it was being treated.…”

Section: Discussionmentioning

confidence: 99%

Influence of Cerebral Vasodilation on Blood Reelin Levels in Growth Restricted Fetuses

et al. 2021

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Fetal growth restriction (FGR) is one of the most important obstetric pathologies. It is frequently caused by placental insufficiency. Previous studies have shown a relationship between FGR and impaired new-born neurodevelopment, although the molecular mechanisms involved in this association have not yet been completely clarified. Reelin is an extracellular matrix glycoprotein involved in development of neocortex, hippocampus, cerebellum and spinal cord. Reelin has been demonstrated to play a key role in regulating perinatal neurodevelopment and to contribute to the emergence and development of various psychiatric pathologies, and its levels are highly influenced by pathological conditions of hypoxia. The purpose of this article is to study whether reelin levels in new-borns vary as a function of severity of fetal growth restriction by gestational age and sex. We sub-grouped fetuses in: normal weight group (Group 1, n = 17), FGR group with normal umbilical artery Doppler and cerebral redistribution at middle cerebral artery Doppler (Group 2, n = 9), and FGR with abnormal umbilical artery Doppler (Group 3, n = 8). Our results show a significant association of elevated Reelin levels in FGR fetuses with cerebral blood redistribution compared to the normal weight group and the FGR with abnormal umbilical artery group. Future research should focus on further expanding the knowledge of the relationship of reelin and its regulated products with neurodevelopment impairment in new-borns with FGR and should include larger and more homogeneous samples and the combined use of different in vivo techniques in neonates with impaired growth during their different adaptive phases.

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Section: Discussionmentioning

confidence: 99%

Influence of Cerebral Vasodilation on Blood Reelin Levels in Growth Restricted Fetuses

et al. 2021

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“…Pregnant women with marginal ID have an important proportion in the women during pregnancy (Ferreira et al, ). There is an increasing concern that marginal ID, a relatively subtle form of TH deficiency, could be harmful to neural development of the offspring (Gilbert et al, ; Liu et al, ; Zhang et al, ). So far, it is still unclear whether marginal ID affects the PCs dendritic growth.…”

Section: Discussionmentioning

confidence: 99%

Maternal marginal iodine deficiency limits dendritic growth of cerebellar purkinje cells in rat offspring by NF‐κB signaling and MAP1B

Dong

Wang

et al. 2016

Environmental Toxicology

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Iodine deficiency (ID) during early pregnancy had an adverse effect on children's psychomotor and motor function. It is worth noting that maternal marginal ID tends to be a common public health problem. Whether marginal ID potentially had adverse effects on the development of cerebellum and the underlying mechanisms remain unclear. Therefore, our aim was to study the effects of marginal ID on the dendritic growth in filial cerebellar Purkinje cells (PCs) and the underlying mechanism. In the present study, we established Wistar rat models by feeding dam rats with a diet deficient in iodine and deionized water supplemented with potassium iodide. We examined the total dendritic length using immunofluorescence, and Western blot analysis was conducted to investigate the activity of nuclear factor-κB (NF-κB) signaling and microtubule-associated protein 1B (MAP1B). Our results showed that marginal ID reduced the total dendritic length of cerebellar PCs, slightly down-regulated the activity of NF-κB signaling and decreased MAP1B in cerebellar PCs on postnatal day (PN) 7, PN14, and PN21. Our study may support the hypothesis that decreased T induced by marginal ID limits PCs dendritic growth, which may involve in the disturbance of NF-κB signaling and MAP1B on the cerebellum. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1241-1251, 2017.

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“…During the first gestational trimester, maternal hypo-thyroxinemia limits the possibilities of postnatal neurodevelopment [27][28][29][30][31][32][33][34][35][36][37]. The most serious form of brain lesion links to neurological cretinism, but mild degrees of maternal hypo-thyroxinemia also produce variations in psychomotor development [38][39][40][41]. The neurologic impairment happens primarily in the second trimester, which is a vital period for formation of the cerebral cortex, the extrapyramidal system, and the cochlea, areas damaged in endemic cretins [42].…”

Section: Maternal Iodine Deficiencymentioning

confidence: 99%

Maternal Iodine Deficiency and Brain Disorders

Rg¹

2016

Endocrinol Metab Syndr

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Thyroid Hormones (THs) play an essential role in development and hormone deficiency during critical phases in fetal life may lead to severe and permanent brain damage. Maternal iodine deficiency is considered the most common cause of fetal TH deficiency, but the problem may also arise in the fetus/neonates. Due to defects in fetal thyroid gland development or hormone synthesis, clinical symptoms at birth are often mild as a result of compensatory maternal TH supply. A shortage of THs starting at the early stages of pregnancy results in neurological deficits that cannot be rescued by exogenous TH addition at later stages. Neonates are more sensitive than adults to the effects of iodine deficiency. Thus, these disturbances may lead to abnormalities in the neuronal network and may result in mental retardation and other neurological defects, including impaired motor skills and visual processing. Thus, iodine defenses programmes can avoid adverse neurodevelopmental consequences in mothers and their offspring.

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Treatment with Iodine in Pregnant Rats with Marginal Iodine Deficiency Improves Cell Migration in the Developing Brain of the Progeny

Cited by 8 publications

References 34 publications

Influence of Cerebral Vasodilation on Blood Reelin Levels in Growth Restricted Fetuses

Influence of Cerebral Vasodilation on Blood Reelin Levels in Growth Restricted Fetuses

Maternal marginal iodine deficiency limits dendritic growth of cerebellar purkinje cells in rat offspring by NF‐κB signaling and MAP1B

Maternal Iodine Deficiency and Brain Disorders

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