Down-regulation of thyroid hormone nuclear receptor levels by l-triiodothyronine in cultured glial C6 cells

Ortiz-Caro, Javier; Montiel, Fatima; Yusta, Bernardo; Pascual, Ángel; Aranda, Ana

doi:10.1016/0303-7207(87)90220-6

Cited by 14 publications

(7 citation statements)

References 18 publications

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“…Several T 3 regulation levels are known to play an important role in maintaining the intracerebral T 3 content that is relatively constant during changes in thyroid status. Thus, increased T 3 concentrations result in depleted TR and type II iodothyronine deiodinase levels and in enhanced activities of type I and III deiodinases, the two enzymes that inactivate T 3 (Ortiz-Caro et al, 1987;Kohrle, 1999). Similar T 3 regulation may occur in fibroblasts and may explain the transitory effects of T 3 treatment on VLCFA ␤-oxidation and ABCD2 expression.…”

mentioning

confidence: 94%

Thyroid Hormone Induction of the Adrenoleukodystrophy-Related Gene (ABCD2)

et al. 2003

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X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VL-CFA) ␤-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3Ј-tri-iodothyronine (T 3 ) receptor (TR␤) as a heterodimer and mediating T 3 responsiveness of ABCD2 in its promoter context. After a T 3 treatment, an induction of the ABCD2 gene was observed in the liver of normal rats but not that of TR␤Ϫ/Ϫ mice. ABCD2 was not induced in the brain of the T 3 -treated rats. However, we report for the first time that induction of the ABCD2 redundant gene is feasible in myelin-producing cells (differentiated CG4 oligodendrocytes). The induction was specific for this cell type because it did not occur in astrocytes. Furthermore, we observed T 3 induction of ABCD2 in human and mouse ABCD1-deficient fibroblasts, which was correlated with normalization of the VLCFA ␤-oxidation. Finally, ABCD3 (PMP70), a close homolog of ABCD2, was also induced by T 3 in the liver of control rats, but not that of TR␤Ϫ/Ϫ mice, and in CG4 oligodendrocytes.

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mentioning

confidence: 94%

Thyroid Hormone Induction of the Adrenoleukodystrophy-Related Gene (ABCD2)

et al. 2003

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“…The remaining nuclear material was extracted twice with 20 mM Tris-HC1, pH 7.5, 1 mM MgC12, 5 mM EDTA, 5 mM DTT, 20 U/ml Trasylol containing 0.4 M KCI and after centrifugation the [12SI]T3 associated to the pellet (crude nuclear matrix) and the supernatant was analyzed. 3. RESULTS digestion during the initial times of digestion demonstrated that the receptor was released 2-3-fold faster than the bulk of chromatin and 20-fold faster than the PCA-soluble fraction.…”

Section: Salt Extraction Of Digested Nucleimentioning

confidence: 97%

“…C6 cells were grown in monolayers as in [3][4][5]. To ensure a complete cellular depletion of thyroid hormone 48 h before the beginning of the experiments the growth medium was replaced by fresh medium containing 10070 newborn calf serum depleted of thyroid hormone [5].…”

Section: C6 Cell Culturementioning

confidence: 99%

“…Parallel cultures were incubated with a 1000-fold excess of non-radioactive T3 to determine the nonspecific binding which was subtracted from the data. The nuclei were isolated [3][4][5] and washed with a buffer containing 10 mM Tris-HC1, pH 7.4 at 25°C, l mM CaClz, 10 mM KC1, 1 mM MgC12, 5 mM 2-mercaptoethanol and 20 U/ml Trasylol. The nuclei were digested with MN (0.25-,0.3 U/I Az6onm U nuclear material) or with DNase I (2-3 U/I A2c, onm U nuclear material) at 0°C as in [2].…”

Section: [~2~i]t3 Labeling and Nuclease Digestion Of Nucleimentioning

confidence: 99%

“…In both systems MN excises the receptor as an abundant 6.5 S form and as a minor Thyroid hormone receptor levels in cells can be influenced by a variety of factors. We have recently demonstrated that in glial C6 cells triiodothyronine (T3) elicits a time-and dose-dependent downregulation of receptors [3]. In contrast to thyroid hormones, butyrate and other short-chain fatty acids increase receptor levels by a mechanism which could involve hyperacetylation of chromatin proteins [4].…”

Section: Introductionmentioning

confidence: 99%

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Organization of the thyroid hormone receptor in the chromatin of C6 glial cells: Evidence that changes in receptor levels are not associated with changes in receptor distribution

et al. 1989

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The association of p25I]T3-receptor complexes with C6 cell chromatin was analyzed after a limited digestion with micrococcal nuclease (MN) or DNase I. Both nucleases solubilized up to 60-70~ of receptor and 0.4 M KCI extracted 70%, of the non-digested receptor, thus showing that only a residual fraction of receptor is associated with the nuclear matriX. With DNase I the receptor was released 2-3-fold faster than the bulk of chromatin, whereas a preferential release of receptor over total chromatin was not observed with MN. The digestion of receptor with DNase I and MN occurred 14-and 6-fold faster, respectively, than the appearance of PCA-soluble chromatin. Preincubation for 48 h with 4 nM T3 of 2 mM butyrate significantly altered receptor levels but did not change sensitivity to the nucleases. These results suggest that the thyroid hormone receptor is associated with chromatin highly sensitive to nuclease digestion, and that changes in receptor number are not associated with changes in its distribution in chromatin.

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Thyroid hormone resistance in hibernating ground squirrels, Spermophilus richardsoni

Magnus

Henderson

1988

General and Comparative Endocrinology

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Down-regulation of thyroid hormone nuclear receptor levels by l-triiodothyronine in cultured glial C6 cells

Cited by 14 publications

References 18 publications

Thyroid Hormone Induction of the Adrenoleukodystrophy-Related Gene (ABCD2)

Thyroid Hormone Induction of the Adrenoleukodystrophy-Related Gene (ABCD2)

Organization of the thyroid hormone receptor in the chromatin of C6 glial cells: Evidence that changes in receptor levels are not associated with changes in receptor distribution

Thyroid hormone resistance in hibernating ground squirrels, Spermophilus richardsoni

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