Thyroid Hormones and 5’-Deiodinase in the Rat Fetus Late in Gestation: Effects of Maternal Hypothyroidism*

Oña, Carmen Ruiz de; Escobar, Gabriella Morreale de; Calvo, Rosa; Rey, Francisco Escobar del; Obregón, Marı́a Jesús

doi:10.1210/endo-128-1-422

Cited by 88 publications

(22 citation statements)

References 46 publications

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“…All these changes associated with cortical development and maturation begin after neurogenesis and strongly suggest that cells trapped in aberrant locations could not later reach their normal destinations, even if an appropriate treatment with iodine or T4 were then instituted. The findings summarized above from the experiment in which dams were treated with methimazole for only 3 days also support this conclusion (38).…”

Section: Figurementioning

confidence: 58%

“…Information obtained for fetuses of thyroidectomized dams (38) revealed that the activity of type II 5′-iodothyronine deiodinase (5′D-II) in the fetal brain was not influenced by maternal thyroidectomy alone and that both T4 and T3 at E17 were decreased, as expected from the decreased maternal circulating levels. When the thyroidectomized dams were given methimazole and fetal thyroid function was impaired, 5′D-II activity did not appear to be upregulated by the decrease in fetal T4 until E19 or later (34,38,39). In the fetuses of LID dams, an increase in 5′D-II activity was also not observed until E19 and was insufficient for the maintenance of normal cerebral T3.…”

Section: Discussionmentioning

confidence: 87%

“…observed in the maternal plasma (31,37,38). Thus, the thyroidectomized dams have very low circulating levels of T4 and T3 up to E21, as do all samples obtained from the conceptus between E9 and E18 -namely, E9-E12 embryotrophoblasts, E9-E12 placentas, and E13-E17 whole embryos.…”

Section: Discussionmentioning

confidence: 98%

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Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Ausó²,

et al. 2003

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Section: Figurementioning

confidence: 58%

Section: Discussionmentioning

confidence: 87%

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Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Ausó²,

et al. 2003

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“…Therefore, it is conceivable that the acquisition of mechanisms of the pit-1 dependent hormonal regulation of gene expression brings about the onset of GH and GHRH-receptor expressions in the developing GH cells. The tissue thyroid hormone level increases rapidly in late gestation in rats [32], and deficiency of T3 due to the administration of anti-thyroid drugs significantly decreases GH cell number and pituitary GH content as well as GH mRNA level in the fetus [9]. T3 also stimulates GHRH-receptor mRNA accumulation in the fetal pituitary in organ culture [8] as well as in adult pituitary gland in vivo [33, 34].…”

Section: Discussionmentioning

confidence: 99%

Regulation of 5′-Promoter Activity of the Rat Growth Hormone and Growth Hormone-Releasing Hormone Receptor Genes in the MtT/S and MtT/E Cells

et al. 2006

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The MtT/E and MtT/S cells have been established from a mammotrophic pituitary tumor, and postulated to be progenitor and premature growth hormone (GH) cells, respectively. The difference in the regulation of GH and GH-releasing hormone (GHRH) receptor gene transcription in relation to the developmental stage of GH cells were examined in these two cell lines. In MtT/S cells, triiodothyronine (T3), all-trans retinoic acid (RA) and 9-cis retinoic acid (9cRA) stimulated GH promoter activity but dexamethasone (DEX) did not. On the other hand, DEX stimulated GHRH-receptor promoter alone. T3, RA and 9cRA showed little effect alone but each of them augmented the effect of DEX when used together with DEX. In MtT/E cells, DEX, RA and 9cRA showed similar effect as observed in MtT/S cells on both GH and GHRH-receptor promoter activity. However, T3 neither stimulated GH promoter activity nor augmented the DEX-induced GHRH-receptor gene transcription in MtT/E cells. RT-PCR analyses revealed that both cell types expressed TRα1, TRβ1 and TRα2, but expression of TRβ2, a pituitary specific isoform of TR, was only detected in MtT/S cells. However, the deficiency of TRβ2 for its own sake does not appear to be a reason why T3 action was not observed in MtT/E cells, because co-transfection of expression plasmids for TRβ2 and RXRα failed in conferring on the cells an ability to respond to T3 by increased GH or GHRH-receptor promoter activity. These results suggest that the acquisition of mechanisms responsible for the regulation of GH or GHRH-receptor transcription by T3 may be involved in the process of functional development of GH cells.

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“…The limits of detection were 2.5 pg T 4 and 1.5 pg T 3 /tube. Cross-reactivities for T 4 and T 3 RIAs were reported previously (Ruiz de Oña et al, 1991). Samples were processed in triplicate, mostly at two dilutions.…”

Section: Determination Of Tissue Thyroid Hormone Concentrationsmentioning

confidence: 99%

The role of type I and type II 5′ deiodinases on hexachlorobenzene-induced alteration of the hormonal thyroid status

et al. 2005

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Thyroid Hormones and 5’-Deiodinase in the Rat Fetus Late in Gestation: Effects of Maternal Hypothyroidism*

Cited by 88 publications

References 46 publications

Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Regulation of 5′-Promoter Activity of the Rat Growth Hormone and Growth Hormone-Releasing Hormone Receptor Genes in the MtT/S and MtT/E Cells

The role of type I and type II 5′ deiodinases on hexachlorobenzene-induced alteration of the hormonal thyroid status

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