Short-term effects of thyroid hormone in prenatal development and cell differentiation

Incerpi, Sandra; Scapin, Sergio; D’Arezzo, Silvia; Spagnuolo, S; Leoni, Silvia

doi:10.1016/j.steroids.2005.02.009

Cited by 37 publications

(33 citation statements)

References 65 publications

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“…T 2 regulates DNA synthesis, cell-cycle proteins (Alisi et al 2004), and several membrane-associated transport systems, whose activity is related to cell proliferation (Incerpi et al 2002(Incerpi et al , 2005. T 2 's effect on the Na C -H C exchanger was identified for 14-day-and 19-dayold cells, whereas the effect on amino acid transport was present at late stages of embryo development.…”

Section: 5-diiodo-l-thyroninementioning

confidence: 99%

Thyroid: biological actions of ‘nonclassical’ thyroid hormones

Senese¹,

Cioffi²,

Lange³

et al. 2014

Journal of Endocrinology

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Thyroid hormones (THs) are produced by the thyroid gland and converted in peripheral organs by deiodinases. THs regulate cell functions through two distinct mechanisms: genomic (nuclear) and nongenomic (non-nuclear). Many TH effects are mediated by the genomic pathway -a mechanism that requires TH activation of nuclear thyroid hormone receptors. The overall nongenomic processes, emerging as important accessory mechanisms in TH actions, have been observed at the plasma membrane, in the cytoplasm and cytoskeleton, and in organelles. Some products of peripheral TH metabolism (besides triiodo-L-thyronine), now termed 'nonclassical THs', were previously considered as inactive breakdown products. However, several reports have recently shown that they may have relevant biological effects. The recent accumulation of knowledge on how classical and nonclassical THs modulate the activity of membrane receptors, components of the mitochondrial respiratory chain, kinases and deacetylases, opened the door to the discovery of new pathways through which they act. We reviewed the current state-of-the-art on the actions of the nonclassical THs, discussing the role that these endogenous TH metabolites may have in the modulation of thyroid-related effects in organisms with differing complexity, ranging from nonmammals to humans.

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Section: 5-diiodo-l-thyroninementioning

confidence: 99%

Thyroid: biological actions of ‘nonclassical’ thyroid hormones

Senese¹,

Cioffi²,

Lange³

et al. 2014

Journal of Endocrinology

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“…Besides TH action mediated by nTRs and involving direct regulation of target gene transcription, a number of rapid TH effects, which cannot be mediated by genomic action and take place outside the nucleus, are becoming increasingly evident (97)(98)(99)(100)(101)(102)(103)(104)(105)(106). These non-genomic responses are often mediated by secondary messengers, such as diacyl glycerol, inositol trisphosphate (IP3), Ca ++ ions and cAMP.…”

Section: Th-binding Sites At the Plasma Membrane And Th Nongenomic Efmentioning

confidence: 99%

“…In L-6 myoblasts and chick embryo hepatocytes, for example, THs have been shown to stimulate, by a non-genomic mechanism, the activity of the Na + /H + exchanger type 1 (NHE-1) (102). NHE-1 is a key phosphoglycoprotein that, besides having a housekeeping role in the maintenance of intracellular pH and cell volume, is involved in regulatory events triggered by different growth-stimulating signals (102). The use of various inhibitors, able to block specific steps of the intracellular signal transduction pathway, has facilitated the demonstration of the involvement of PKC and the MAPK pathway in the activation of NHE-1 by THs (113).…”

Section: Th-binding Sites At the Plasma Membrane And Th Nongenomic Efmentioning

confidence: 99%

“…The use of various inhibitors, able to block specific steps of the intracellular signal transduction pathway, has facilitated the demonstration of the involvement of PKC and the MAPK pathway in the activation of NHE-1 by THs (113). Through the formation of IP3, THs also mobilize intracellular calcium ions (102). In a rat pituitary cell line, THs stimulated phosphatidylinositol 3-kinase (PI3K) and Rac activity, which in turn stimulated voltageactivated potassium channels (83,114).…”

Section: Th-binding Sites At the Plasma Membrane And Th Nongenomic Efmentioning

confidence: 99%

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Thyroid hormones and the central nervous system of mammals (Review)

Liegro

2008

Mol Med Report

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Abstract. The thyroid hormones (THs) L-thyroxine (T4) and L-triiodothyronine (T3) have a profound influence on the development and maturation of the mammalian brain, both before and after birth. Any impairment in the supply of THs to the developing nervous system leads to severe and irreversible changes in both the overall architecture and functions of the brain and causes, in humans, neurological and motor deficits known as cretinism. Pronounced neurological symptoms are also commonly observed in adult patients suffering from both hyperthyroidism and hypothyroidism, and it has recently emerged that certain symptoms might result from the reduced brain uptake, rather than the insufficient production, of THs. Most of the effects of THs are mediated by two classes of nuclear receptors (α and ß isoforms), which belong to the c-erbA superfamily of transcriptional regulators and are expressed in a tissue-specific and developmentally regulated manner. Interestingly, the nuclear TH receptors (nTRs) act as both ligand-independent gene repressors and ligand-dependent gene activators. On the other hand, negatively-regulated genes, which can be stimulated in the absence of THs and repressed by THs, have also been observed. Due to this complex pattern of regulation, the effects of receptor dysfunction do not exactly overlap the effects of hormone deficiency or excess. Moreover, non-genomic mechanisms of TH action have been described in many tissues, including the brain, some of which seem to be mediated by integrins and to be calcium-dependent. Intracellular receptors, distinct from nTRs, are present in the mitochondria, where a matrix-associated, T3-dependent transcriptional regulator of approximately 43 kDa has been described. Finally, complex patterns of pituitary and/or peripheral resistance to thyroid hormones (RTH), characterized by elevated plasma levels of THs and non-suppressible thyroidstimulating hormone (TSH), have been identified. This review summarizes the major advances in knowledge of the molecular mechanisms of TH action and their implication for the effects of THs on the developing, as well as the adult mammalian, nervous system.

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“…On account of TH action can be controlled in individual cells through selective TH uptake and intracellular TH metabolism, the placenta is an important link in the maternal-fetal communication network for THs which are essential for the normal development and differentiation of the fetus [1][2][3]. Generally, intracellular activation or inactivation of Lthyroxine (T4) and 3,5,3'-triiodothyronine (T3) in turn is determined by three types of iodothyronine deiodinases (Ds), namely DI, DII, and DIII [4][5][6][7]. The placenta transports and metabolizes maternal THs, and mainly expresses DIII, which inactivates T4 and other iodothyronines and thus limits the transfer of maternal active THs to the fetus in the late pregnancy [8].…”

Section: Introductionmentioning

confidence: 99%

Maternal-Fetal Thyroid Interactions

Ahmed¹

2012

Thyroid Hormone

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Short-term effects of thyroid hormone in prenatal development and cell differentiation

Cited by 37 publications

References 65 publications

Thyroid: biological actions of ‘nonclassical’ thyroid hormones

Thyroid: biological actions of ‘nonclassical’ thyroid hormones

Thyroid hormones and the central nervous system of mammals (Review)

Maternal-Fetal Thyroid Interactions

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