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Thyroid hormone receptor beta (THRβ1) is the major regulator of T3 action in human iPSC-derived hepatocytes

ABSTRACT: Thyroid hormone receptor beta (THRβ1) is the major regulator of T3 action in human iPSC-derived hepatocytes

PROVIDER: PRJNA1125486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29457821_1.fastq.gz	Fastqsanger.gz
	SRR29457821_2.fastq.gz	Fastqsanger.gz
	SRR29457822_1.fastq.gz	Fastqsanger.gz
	SRR29457822_2.fastq.gz	Fastqsanger.gz
	SRR29457823_1.fastq.gz	Fastqsanger.gz

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Thyroid hormone receptor beta (THRβ1) is the major regulator of T3 action in human iPSC-derived hepatocytes

Project description:To investigate the role of THRβ1 action in human iPSC-derived hepatocytes. We then performed gene expression profiling analysis using data obtained from RNA-seq of WT and THRBKO human iPSCs-derived hepatocytes in presence and absence of T3.

2024-11-01 | GSE270233 | GEO

Digital Gene Expression (DGE) of thyroid hormone (T3)-responsive genes in C17.2 cells stably transfected with thyroid hormone receptors alpha and beta

Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. Cells were treated with 10-7 M T3 for 6, 12 or 24h or left untreated. We performed DGE by sequencing all polyA RNA according to a SAGE-derived method. Differential gene expression after T3 treatment was computed and the T3 responses induced by the two receptors were compared. We could conclude that, in a similar environment, target genes are only partially shared and that a significant proportion show receptor preference and even selectivity. Examination of thyroid hormone target genes over time in two cell lines (C17.2a, C17.2b), each expressing one of the thyroid hormone receptors (alpha, beta).

2012-12-31 | E-GEOD-38539 | biostudies-arrayexpress

Identical gene regulation patterns of triiodothyronine (T3) and selective thyroid hormone receptor modulator GC-1

Project description:This SuperSeries is composed of the following subset Series: GSE32443: Identical gene regulation patterns of triiodothyronine (T3) and selective thyroid hormone receptor modulator GC-1 [Affymetrix] GSE32444: Identical gene regulation patterns of triiodothyronine (T3) and selective thyroid hormone receptor modulator GC-1 [Illumina] Refer to individual Series

2011-10-31 | E-GEOD-32445 | biostudies-arrayexpress

Thyroid hormone action in human hepatocytes and the Cistromes of TRB1 and ChREBP in liver of mice

Project description:Human iPSC were differentiated to hepatocytes and treated with T3 or vehicle then total RNA was sequenced. The cistrome of TRB1 or ChREBP was delineated in liver of hypothyroid and hyperthyroid mice.

2021-11-16 | GSE133110 | GEO

Digital Gene Expression (DGE) of thyroid hormone (T3)-responsive genes in C17.2 cells stably transfected with thyroid hormone receptors alpha and beta

2012-12-31 | GSE38539 | GEO

Triiodothyronine (T3) promotes brown fat hyperplasia via thyroid hormone receptor α mediated adipocyte progenitor cell proliferation

Project description:The thyroid hormone (TH)-controlled recruitment process of brown adipose tissue (BAT) is not fully understood. Here, we show that long-term treatment of T3, the active form of TH, increases the recruitment of thermogenic capacity in interscapular BAT of male mice through hyperplasia by promoting the TH receptor α-mediated adipocyte progenitor cell proliferation. Our single-cell analysis reveals the heterogeneous nature and hierarchical trajectory within adipocyte progenitor cellsof interscapular BAT. Further analyses suggest that T3 facilitates cell state transition from a more stem-like state towards a more committed adipogenic state and promotes cell cycle progression towards a mitotic state in adipocyte progenitor cells, through mechanisms involving the action of Myc on glycolysis. Our findings elucidate the mechanisms underlying the TH action in adipocyte progenitors residing in BAT and provide a framework for better understanding of the TH effects on hyperplastic growth and adaptive thermogenesis in BAT depot at a single-cell level.

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Effect of v-erbA on T3-responsive genes in AML-12 hepatocytes

Project description:The v-erbA oncogene belongs to a superfamily of transcription factors called nuclear receptors, which includes the thyroid hormone receptors (TRs) responsible for mediating the effects of thyroid hormone (T3). Nuclear receptors bind to specific DNA sequences in the promoter region of target genes and v-erbA is known to exert a dominant negative effect on the activity of the TRs. The repressor activity of v-erbA has been linked to the development of hepatocellular carcinoma (HCC) in a mouse model. We have used microarray analysis to identify genes differentially expressed in hepatocytes in culture (AML12 cells) stably transfected with v-erbA and exposed to T3. We have found that v-erbA can negatively regulate expression of T3-responsive genes known to have a protective function against tumor development. We have also identified a number of v-erbA- (but not T3-) responsive genes that are known to be involved in carcinogenesis and which may play a role in the development of HCC.

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Regulation of Gene Expression by Thyroid Hormone in Cultured Astrocytes: Transcriptional Targets and Factors Influencing the Genomic Response

Project description:Astrocytes mediate the action of thyroid hormone in the brain on other neural cells through the production of the active hormone triiodothyronine (T3) from its precursor thyroxine (T4). T3 has also many effects on the astrocytes in vivo and in culture, but whether these actions are directly mediated by transcriptional regulation is not clear. In this work, we have analyzed the genomic response to T3 of cultured astrocytes isolated from the postnatal mouse cerebral cortex, using RNA sequencing. Cultured astrocytes express relevant genes of thyroid hormone metabolism and action encoding type 2 deiodinase (Dio2), Mct8 transporter (Slc16a2), T3 receptors (Thra1 and Thrb), and nuclear corepressor (Ncor1) and coactivator (Ncoa1). T3 changed the expression of 668 genes (4.5% of expressed genes), of which 117 genes (0.8% of expressed genes) were primary, transcriptional responses. The Wnt and Notch pathways were down-regulated at the post-transcriptional level. Comparison with the effect of T3 on astrocyte-enriched genes in mixed cerebrocortical cultures isolated from fetal cortex revealed that the response to T3 is influenced by the degree of astrocyte maturation, and that in agreement with its physiological effects, T3 promotes the transition between the fetal and adult patterns of gene expression.

2018-08-21 | GSE110372 | GEO

Thyroid Hormone Dependent Transcriptional Programming by TRb Requires SWI/SNF Chromatin Remodelers

Project description:Transcriptional regulation in response to thyroid hormone (3,5,3´-triiodo-L-thyronine, T3) is a dynamic and cell-type specific process that maintains cellular homeostasis and identity in all tissues. However, our understanding of the mechanisms of thyroid hormone receptor (TR) actions at the molecular level are actively being refined. We used an integrated genomics approach to profile and characterize the cistrome of TRb, map changes in chromatin accessibility, and capture the transcriptomic changes in response to T3 in normal human thyroid cells. There are significant shifts in TRb genomic occupancy in response to T3, which are associated with differential chromatin accessibility, and differential recruitment of SWI/SNF chromatin remodelers. We further demonstrate selective recruitment of BAF and PBAF SWI/SNF complexes to TRb binding sites, revealing novel differential functions in regulating chromatin accessibility and gene expression. Our findings highlight three distinct modes of TRb interaction with chromatin and coordination of coregulator activity.

2022-04-04 | PXD030403 | Pride

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