Effect of Different Iodine Nutrition on Cerebellum Pcp-2 in Rat Offspring During Lactation

Lu, Zhigang; Sun, Yi; Li, Yong Mei; Lin, Lai Xiang; Yan, Ye; Yan, Yu; Chen, Zu Pei

doi:10.1007/s12011-011-8991-3

Cited by 7 publications

(8 citation statements)

References 33 publications

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“…Zhang et al also undertook a study on the effect of differing nutritional iodine levels on cerebellum Purkinje cells, but observed no significant change in the expression of Purkinje cell protein-2 in a mildly iodine-deficient group [104]. It is supposed that the daily iodine intake for the mildly iodinedeficient rats was a little higher (5 μg/day), and the thyroid hormone levels of mildly iodine-deficient rats did not change compared with controls.…”

Section: Cerebellummentioning

confidence: 99%

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

et al. 2015

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Maternal hypothyroxinemia can induce neurodevelopmental impairments in the developing fetus. We here review recent studies on the epidemiology and molecular mechanisms associated with this important public health issue. In 2011, the American Thyroid Association defined maternal hypothyroxinemia as low serum free thyroxine (FT4) levels (<5th or <10th percentile) existing in conjunction with normal serum free triiodothyronine (FT3) or thyroid stimulating hormone (TSH) levels during pregnancy. Compared to clinical or subclinical hypothyroidism, hypothyroxinemia is more commonly found in pregnant women. Hypothyroxinemia usually ensues in response to several factors, such as mild iodine deficiency, environmental endocrine disrupters, or certain thyroid diseases. Unequivocal evidence demonstrates that maternal hypothyroxinemia leads to negative effects on fetal brain development, increasing the risks for cognitive deficits and poor psychomotor development in resulting progeny. In support of this, rodent models provide direct evidence of neurodevelopmental damage induced by maternal hypothyroxinemia, including dendritic and axonal growth limitation, neural abnormal location, and synaptic function alteration. The neurodevelopmental impairments induced by hypothyroxinemia suggest an independent role of T4. Increasing evidence indicates that adequate thyroxine is required for the mothers in order to protect against the abnormal brain development in their progeny.

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Section: Cerebellummentioning

confidence: 99%

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

et al. 2015

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“…Fetus and infants are at the highest risk of iodine deficiency among the population [34]. Maternal hypothyroidism and hypothyroxenaemia impair brain development of the newborn severely [7,35]. Therefore, in the present study, we gave the rats the treatments to induce hypothyroidism during pregnancy and lactation (from GD6 to PN28), in an attempt to mimic the effects of developmental iodine deficiency and hypothyroidism on cerebellar development.…”

Section: Discussionmentioning

confidence: 99%

Developmental Iodine Deficiency and Hypothyroidism Impair Neural Development, Upregulate Caveolin-1, and Downregulate Synaptotagmin-1 in the Rat Cerebellum

Wang

Zhong

Wei

et al. 2011

Biol Trace Elem Res

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Adequate thyroid hormone is critical for cerebellar development. Developmental hypothyroidism induced by iodine deficiency during gestation and postnatal period results in permanent impairments of cerebellar development with an unclear mechanism. In the present study, we implicate cerebellar caveolin-1 and synaptotagmin-1, the two important molecules involved in neuronal development, in developmental iodine deficiency, and in developmental hypothyroidism. Two developmental rat models were created by administrating dam rats with either iodine-deficient diet or propylthiouracil (PTU, 5 or 15 ppm)-added drinking water from gestational day 6 till postnatal day (PN) 28. Nissl staining and the levels of caveolin-1 and synaptotagmin-1 in cerebella were assessed on PN28 and PN42. The results show that the numbers of Purkinje cells were reduced in the iodine-deficient and PTU-treated rats. The upregulation of caveolin-1 and the downregulation of synaptotagmin-1 were observed in both iodine-deficient and PTU-treated rats. These findings may implicate decreases in the number of Purkinje cells and the alterations in the levels of caveolin-1 and synaptotagmin-1 in the impairments of cerebellar development induced by developmental iodine deficiency and hypothyroidism.

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“…The amniotic fluid sample of per dam was pooled over six fetuses. Thyrotropin (TSH) and THs in serum samples were measured by a chemiluminescent immunoassay technique that we have reported previously [29].…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA of normal rat placenta (2 µg) and of the extracted LCM samples (0.2 µg) was reverse-transcribed to complementary DNA as previously described [29].…”

Section: Methodsmentioning

confidence: 99%

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Expression of Organic Anion Transporting Polypeptide 1c1 and Monocarboxylate Transporter 8 in the Rat Placental Barrier and the Compensatory Response to Thyroid Dysfunction

et al. 2014

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Thyroid hormones (THs) must pass from mother to fetus for normal fetal development and require the expression of placental TH transporters. We investigate the compensatory effect of placental organic anion transporting polypeptide 1c1 (Oatp1c1) and monocarboxylate transporter 8 (Mct8) on maternal thyroid dysfunction. We describe the expressions of these two transporters in placental barriers and trophoblastic cell populations in euthyroidism and thyroid dysfunction resulting from differential iodine nutrition at gestation day (GD) 16 and 20, that is, before and after the onset of fetal thyroid function. Immunohistochemistry revealed that in the blood-placenta barrier, these two TH transporters were strongly expressed in the villous interstitial substance and were weakly expressed in trophoblast cells. Levels of Oatp1c1 protein obviously increased in the placental fetal portion during maternal thyroid deficiency at GD16. Under maternal thyroid deficiency after the production of endogenous fetal TH, quantitative PCR analysis revealed down-regulation of Oatp1c1 occurred along with up-regulation of Mct8 in trophoblast cell populations isolated by laser capture microdissection (LCM); this was consistent with the protein levels in the fetal portion of the placenta. In addition, decreased D3 mRNA at GD16 and increased D2 mRNA on two gestational days were observed in trophoblast cells with thyroid dysfunction. However, levels of Oatp1c1 mRNA at GD16 and D3 mRNA at GD20 were too low to be detectable in trophoblast cells. In conclusion, placental Oatp1c1 plays an essential compensatory role when the transplacental passage of maternal THs is insufficient at the stage before the fetal TH production. In addition, the coordinated effects of Oatp1c1, Mct8, D2 and D3 in the placental barrier may regulate both transplacental TH passage and the development of trophoblast cells during thyroid dysfunction throughout the pregnancy.

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Effect of Different Iodine Nutrition on Cerebellum Pcp-2 in Rat Offspring During Lactation

Cited by 7 publications

References 33 publications

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

Developmental Iodine Deficiency and Hypothyroidism Impair Neural Development, Upregulate Caveolin-1, and Downregulate Synaptotagmin-1 in the Rat Cerebellum

Expression of Organic Anion Transporting Polypeptide 1c1 and Monocarboxylate Transporter 8 in the Rat Placental Barrier and the Compensatory Response to Thyroid Dysfunction

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