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3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of K562 cells treated with DMSO and TRIAC

ORGANISM(S): Homo sapiens

PROVIDER: GSE165769 | GEO | 2024/01/01

REPOSITORIES: GEO

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3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α.

Project description:The human ζ-globin gene (HBZ) is transcribed in primitive erythroid cells only during the embryonic stages of development. Reactivation of this embryonic globin synthesis would likely alleviate symptoms both in α-thalassemia and sickle-cell disease. However, the molecular mechanisms controlling ζ-globin expression have remained largely undefined. Moreover, the pharmacologic agent capable of inducing ζ-globin production is currently unavailable. Here, we show that TRIAC, a bioactive thyroid hormone metabolite, significantly induced ζ-globin gene expression during zebrafish embryogenesis. The induction of ζ-globin expression by TRIAC was also observed in human K562 erythroleukemia cell line and primary erythroid cells. Thyroid hormone receptor α (THRA) deficiency abolished the ζ-globin-inducing effect of TRIAC. Furthermore, THRA could directly bind to the distal enhancer regulatory element to regulate ζ-globin expression. Our study provides the first evidence that TRIAC acts as a potent inducer of ζ-globin expression, which might serve as a new potential therapeutic option for patients with severe α-thalassemia or sickle-cell disease.

| S-EPMC8235803 | biostudies-literature

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α.

| S-EPMC8235803 | biostudies-literature

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-01 | GSE165770 | GEO

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

Project description:To characterize genome-wide THRA traget genes in K562 cells.

2024-01-01 | GSE165768 | GEO

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

| PRJNA697855 | ENA

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

| PRJNA697859 | ENA

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

| PRJNA697860 | ENA

Retinoic acid induces expression of the thyroid hormone transporter, monocarboxylate transporter 8 (Mct8).

Project description:Retinoic acid (RA) and thyroid hormone are critical for differentiation and organogenesis in the embryo. Mct8 (monocarboxylate transporter 8), expressed predominantly in the brain and placenta, mediates thyroid hormone uptake from the circulation and is required for normal neural development. RA induces differentiation of F9 mouse teratocarcinoma cells toward neurons as well as extraembryonal endoderm. We hypothesized that Mct8 is functionally expressed in F9 cells and induced by RA. All-trans-RA (tRA) and other RA receptor (RAR) agonists dramatically (>300-fold) induced Mct8. tRA treatment significantly increased uptake of triiodothyronine and thyroxine (4.1- and 4.3-fold, respectively), which was abolished by a selective Mct8 inhibitor, bromosulfophthalein. Sequence inspection of the Mct8 promoter region and 5'-rapid amplification of cDNA ends PCR analysis in F9 cells identified 11 transcription start sites and a proximal Sp1 site but no TATA box. tRA significantly enhanced Mct8 promoter activity through a consensus RA-responsive element located 6.6 kilobases upstream of the coding region. A chromatin immunoprecipitation assay demonstrated binding of RAR and retinoid X receptor to the RA response element. The promotion of thyroid hormone uptake through the transcriptional up-regulation of Mct8 by RAR is likely to be important for extraembryonic endoderm development and neural differentiation. This finding demonstrates cross-talk between RA signaling and thyroid hormone signaling in early development at the level of the thyroid hormone transporter.

| S-EPMC2930727 | biostudies-literature

Thyroid hormone induces cerebellar Purkinje cell dendritic development via the thyroid hormone receptor alpha1.

Project description:The thyroid hormone l-3,3',5-triiodothyronine (T3) plays an important role during cerebellar development. Perinatal T3 deficiency leads to severe cellular perturbations, among them a striking reduction in the growth and branching of Purkinje cell dendritic arborization. The molecular mechanisms underlying these effects are poorly understood. Despite the well documented broad expression of thyroid hormone receptors (TRs), analysis of different TR-deficient mice has failed to provide detailed information about the function of distinct TRs during neuronal development. The cerebellar cell culture systems offer an excellent model by which to study the effects of T3, because differentiation of cerebellar neurons in mixed and purified cultures proceeds in the absence of serum that contains T3. Addition of T3 to cerebellar cultures causes a dramatic increase in Purkinje cell dendrite branching and caliber in a dose- and time-dependent manner. Furthermore, we demonstrate for the first time that T3 acts on Purkinje cells directly through TRalpha1 expressed on the Purkinje cell and not on the granule cell, the presynaptic partner of Purkinje cells. In contrast, TRbeta isoforms are not involved, because Purkinje cells derived from TRbeta-/- mice show the same T3 responsiveness as wild-type cells. T3-promoted Purkinje cell differentiation was not mediated via neurotrophins, as suggested previously, because dendritogenesis of Purkinje cells from BDNF-/- mice could be effectively stimulated in vitro by T3 treatment. Furthermore, the effects of T3 observed were not abolished by tyrosine kinase receptor B (TrkB)-IgG, TrkC-IgG, or K252a, agents known to block the actions of neurotrophin. These results indicate that T3 directly affects Purkinje cell differentiation through activation of the TRalpha1.

| S-EPMC6740935 | biostudies-literature

Increased sensitivity to thyroid hormone in mice with complete deficiency of thyroid hormone receptor alpha.

Project description:Only three of the four thyroid hormone receptor (TR) isoforms, alpha1, beta1, and beta2, bind thyroid hormone (TH) and are considered to be true TRs. TRalpha2 binds to TH response elements on DNA, but its role in vivo is still unknown. We produced mice completely deficient in TRalpha (TRalpha(o/o)) that maintain normal serum thyroid-stimulating hormone (TSH) concentration despite low serum thyroxine (T(4)), suggesting increased sensitivity to TH. We therefore examined the effects of TH (L-3,3',5-triiodothyronine, L-T3) given to TH-deprived and to intact TRalpha(o/o) mice. Controls were wild-type (WT) mice of the same strain and mice resistant to TH due to deficiency in TRbeta (TRbeta(-/-)). In liver, T3 produced significantly greater responses in TRalpha(o/o) and smaller responses in TRbeta(-/-) as compared with WT mice. In contrast, cardiac responses to L-T3 were absent or reduced in TRalpha(o/o), whereas they were similar in WT and TRbeta(-/-) mice, supporting the notion that TRalpha1 is the dominant TH-dependent TR isoform in heart. 5-Triiodothyronine (L-T3) given to intact mice produced a greater suppression of serum T(4) in TRalpha(o/o) than it did in WT mice and reduced by a greater amount the TSH response to TSH-releasing hormone. This is an in vivo demonstration that a TR deficiency can enhance sensitivity to TH. This effect is likely due to the abrogation of the constitutive "silencing" effect of TRalpha2 in tissues expressing the TRbeta isoforms.

| S-EPMC14593 | biostudies-literature

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