Identification of new thyroid hormone-regulated genes in rat brain neuronal cultures

Martel, J.C.; Cayrou, Christelle; Puymirat, Jack

doi:10.1097/00001756-200210280-00003

Cited by 29 publications

(16 citation statements)

References 10 publications

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“…Therefore, an indirect regulation of nNOS expression in the cerebral cortex might not to be excluded during hyperthyroidism. The consensus sequence of TRE was not described in the nNOS promoter [3], and studies using microarray technique did not confirm the direct regulation of nNOS by TH either [22][23][24]. The latter finding implicate that the effect of TH on nNOS production, and hence activity, may occur via indirect, nongenomic pathways.…”

Section: Possible Regulatory Mechanisms Of Nnos By Thmentioning

confidence: 93%

Thyroid Hormones affect the Level and Activity of Nitric Oxide Synthase in Rat Cerebral Cortex during Postnatal Development

et al. 2007

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The effects of thyroid hormones (TH) on the enzyme level and activity of neuronal nitric oxide synthase (nNOS) were studied in the rat cerebral cortex during postnatal life. As revealed by arginine/citrulline conversion assay and Western blot analysis of the homogenate of the parietal cortex T4 significantly increased nNOS activity and nNOS protein level to 153 +/- 25% and to 178 +/- 20%, respectively. In contrast, 6-n-propyl-2-thyouracil (PTU) decreased nNOS activity and nNOS level to 45 +/- 10% and to 19 +/- 4%, respectively. The number of nNOS-immunoreactive neurons did not change after either T4 or PTU treatment, however, following T4 administration the percentage of intensively immunoreactive neurons increased to 85 +/- 3% compared to control (65 +/- 6%), whereas it decreased to 49 +/- 2% after PTU treatment. Our findings indicate that abnormal TH levels differentially regulate the activity and the level of nNOS and suggest a cross-talk between the TH and NO signaling pathway in the developing cerebral cortex of rats.

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Section: Possible Regulatory Mechanisms Of Nnos By Thmentioning

confidence: 93%

Thyroid Hormones affect the Level and Activity of Nitric Oxide Synthase in Rat Cerebral Cortex during Postnatal Development

et al. 2007

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“…Klf9 is a T 3 target gene in several neuronal cell types (16,17). It encodes a transcription factor identified as an inhibitor of axonal regeneration in murine retinal ganglion cells (5).…”

Section: Krüppel-like Factor 9 Mediates the Inhibitory Effect Of T 3 mentioning

confidence: 99%

“…We therefore investigated the involvement of high T 3 levels in the onset of the loss of regenerative capacity of postnatal PCs. Because Krüppel-like factor 9 (Klf9) is a transcriptional target of T 3 in some neuronal cell types (16,17) and is involved in the developmental loss of regenerative ability of retinal ganglion cells (5), we also examined whether T 3 acts on PCs by regulating Klf9 expression.…”

mentioning

confidence: 99%

Thyroid hormone triggers the developmental loss of axonal regenerative capacity via thyroid hormone receptor α1 and krüppel-like factor 9 in Purkinje cells

Avci

Lebrun

Wehrlé

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Neurons in the CNS of higher vertebrates lose their ability to regenerate their axons at a stage of development that coincides with peak circulating thyroid hormone (T 3 ) levels. Here, we examined whether this peak in T 3 is involved in the loss of axonal regenerative capacity in Purkinje cells (PCs). This event occurs at the end of the first postnatal week in mice. Using organotypic culture, we found that the loss of axon regenerative capacity was triggered prematurely by early exposure of mouse PCs to T 3 , whereas it was delayed in the absence of T 3 . Analysis of mutant mice showed that this effect was mainly mediated by the T 3 receptor α1. Using gain-and loss-of-function approaches, we also showed that Krüppel-like factor 9 was a key mediator of this effect of T 3 . These results indicate that the sudden physiological increase in T 3 during development is involved in the onset of the loss of axon regenerative capacity in PCs. This loss of regenerative capacity might be part of the general program triggered by T 3 throughout the body, which adapts the animal to its postnatal environment.axon regeneration | cerebellum | neural development | lentiviral vectors

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“…The first three genes are up-regulated and the last one down-regulated by T3 (201). Moreover, by comparing the gene expression profiles of control newborn mice at the 4th postnatal day (P4) with age-matched experimentally hypothyroid mice and hypothyroid mice treated with tiroxine, Takahashi et al (202) identified six novel TH-responsive genes expressed in the developing cerebellum: orc11, galr3, sort1, nlgn3, cdk5r2 and zfp367.…”

Section: Ontogenesis Of Th Receptors In the Brainmentioning

confidence: 99%

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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Identification of new thyroid hormone-regulated genes in rat brain neuronal cultures

Cited by 29 publications

References 10 publications

Thyroid Hormones affect the Level and Activity of Nitric Oxide Synthase in Rat Cerebral Cortex during Postnatal Development

Thyroid Hormones affect the Level and Activity of Nitric Oxide Synthase in Rat Cerebral Cortex during Postnatal Development

Thyroid hormone triggers the developmental loss of axonal regenerative capacity via thyroid hormone receptor α1 and krüppel-like factor 9 in Purkinje cells

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

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