Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional analysis of THs-responding genes during human hepatocyte development

ABSTRACT: Liver is one of the major targets of thyroid hormones (THs), as well as many industrial chemicals reported as THs-analogues. A number of THs-analogues could permeate the placenta barrier, risking the embryonic development, which may be more susceptible and cause sustained health risk. Therefore, to study the toxicology of industrial chemicals during the hepatocytes developmental stage is necessary, and may be more efficiency. In this study, we differentiated human embryonic stem cells (hESCs) into functional hepatocyte-like cells in presence of two thyroid hormones (THs, T3 and T4), with the purposes trying to dissect genes regulated by THs during human hepatocyte development and identifying biomarkers for THs-analogues. THs exposure finally induced dysfunctional hepatocytes with 19 days differentiation, with impaired glycogen storage ability and lipid droplets accumulation. Global gene expression analysis by RNA-seq identified a number of genes responding to THs were responsible for hepatic differentiation and function, enriched in many metabolic related pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE124017 | GEO | 2020/12/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Thyroid Hormone effects on hiPSC-derived cardiomyocytes (hiPSC-CM). Identification of target genes and pathways by RNA-Seq analysis

Project description:QT prolongation represents a dangerous and potentially life-threatening electrical event affecting the heart. Thyroid hormones (THs) are critical for cardiac development and heart function. However, little is known about THs influence on ventricular repolarization and controversial effects on QT prolongation are reported. Aim of this study was to characterize the direct effects of THs on the cardiac repolarization of human Induced Pluripotent Stem Cell derived cardiomyocytes (hiPSC-CM). RNA Seq analysis of hiPSC-CM treated with Thyroid Hormone T3 indicates significant deregulation in genes involved in cardiac pathways, in particular in ion homeostasis.

2021-12-08 | GSE172348 | GEO

Characterization of Directly Regulated Thyroid Hormone Mediated Gene Expression Following Short-Term Perturbations in Thyroid Hormone Levels in Juvenile Mice

Project description:We investigated the effects of thyroid hormone disruptions on gene expression in juvenile mice liver to develop a stronger understanding of the mechanisms by which thyroid disrupting chemicals impair development. Gene expression was examined by hybridization of hepatic RNA to Agilent mouse microarrays for hyper-, hypo-, hypo-replacement (hypo+) and euthyroid animals. Keywords: Toxicogenomics, biomarkers of thyroid disruptors Hypothyroidism was induced from post natal day (PND) 13 to 15 by adding model thyroid toxicants methimazole and sodium perchlorate to drinking water of pregnant females. Hyperthyroidism was induced by intraperitoneal injections (i.p.) of THs at PND 15, 4 hours before decapitation and tissue collection. For the hypothyroid/replacement group; dams were provided with drinking water for 3 days (PND 13 to 15), containing a mixture of methimazole/sodium perchlorate. Pups then received intraperitoneal injections of thyoid hormones on PND 15, 4 hours before decapitation and tissue collection.

2012-03-29 | E-GEOD-21307 | biostudies-arrayexpress

Integrin αvβ3 acting as membrane receptor for thyroid hormones mediates angiogenesis in malignant T cells

2015-02-18 | GSE63122 | GEO

Molecular analysis of endocrine disruption in hornyhead turbot captured from wastewater treatment plant discharge locations in Southern California

Project description:Hornyhead turbot (Pleuronichthys verticalis) captured near sewage outfalls are used as sentinel fish for monitoring exposure to industrial and agricultural chemicals of ~20 million people living in coastal southern California. Although analyses of hormones in blood and organ morphology and histology in fish are useful for assessing exposure, there is a need for quantitative and sensitive molecular measurements, as many contaminants produce subtle effects. A novel multispecies microarray and qRT-PCR were used to investigate endocrine disruption in turbot captured near sewage outfalls in San Diego, Orange County and Los Angeles California. Analysis of expression of genes involved in hormone [e.g. estrogen, androgen, thyroid] responses and xenobiotic metabolism in turbot livers was correlated with phenotypic end points.

2013-12-10 | E-MEXP-3852 | biostudies-arrayexpress

Effects of Acute Exposure to the Non-steroidal Anti-inflammatory Drug Ibuprofen on the Developing North American Bullfrog (Rana catesbeiana) Tadpole

Project description:An anthropogenic chemical contaminant commonly identified in aquatic receiving environments is the non-steroidal anti-inflammatory drug (NSAID), ibuprofen(IBF). While the role of ibuprofen in target organisms is known, there exists a paucity of data on the impact of exposure to non-target wildlife species. In the case of frog species, normal development and environmental fitness involves the actions of the thyroid hormones (THs), particularly at key points in the life cycle. We investigated whether exposure of premetamorphic North American bullfrog (Rana catesbeiana) tadpoles to IBF altered their response to treatment with an exogenous dose of thyroid hormone (T3).

2014-09-23 | GSE53565 | GEO

Integrin αvβ3 acting as membrane receptor for thyroid hormones mediates angiogenesis in malignant T cells

Project description:We have found that thyroid hormones (THs), acting as soluble integrin αvβ3 ligands, activate growth-related signaling pathways in T-cell lymphomas (TCL). Specifically, TH-activated αvβ3 integrin signaling promotes TCL proliferation and angiogenesis, in part, via the up-regulation of VEGF. CUTLL1 cells were treated with T3- and T4-bound agarose or agarose alone for 24hrs. Total RNA was harvested from cells and used for expression profiling via RNA-seq.

2015-02-18 | E-GEOD-63122 | biostudies-arrayexpress

Thyroid hormone receptor beta (THRB) dependent regulation of diurnal hepatic lipid metabolism in adult male mice

Project description:Thyroid hormones (THs) are critical regulators of systemic energy metabolism and homeostasis. In the liver, high TH action protects against steatosis by enhancing cholesterol and triglyceride turnover, with thyroid hormone receptor beta (THRB) signaling playing a pivotal role. This study probed the potential interaction between THRB action and another critical regulator of liver energy metabolism, the circadian clock. Liver transcriptome analysis of THRB deficient (THRBKO) mice under normal chow conditions revealed a markedly modest impact of THRB deletion. Temporal transcriptome and lipidome profiling uncovered significant alterations in diurnal metabolic rhythms attributable to THRB deficiency pointing to a pro-steatotic state with elevated levels of cholesterol, tri- and diacylglycerides, and fatty acids. These findings were confirmed by THRB agonization in hepatocytes under steatosis-promoting conditions in vitro. Integration of transcriptome profiles from THRBKO mice and mice with induced high or low TH action identified a subset of TH responsive but THRB insensitive genes implicated in immune processes. In summary, our study reveals a complex time-of-day dependent interaction of different TH-related signals in the regulation of liver physiology indicating an opportunity for chronopharmacological approaches to TH/THR(B) manipulation in fatty liver diseases.

2024-08-13 | GSE254467 | GEO

Effects of Acute Exposure to the Non-steroidal Anti-inflammatory Drug Ibuprofen on the Developing North American Bullfrog (Rana catesbeiana) Tadpole

2014-09-23 | E-GEOD-53565 | biostudies-arrayexpress

Early target genes of aflatoxin B1 in human hepatic cells

Project description:Comparison of gene expression profiles induced by the mycotoxin, aflatoxin B1 (AFB1), in primary human hepatocytes and HepaRG cells. Initial mechanisms involved in the complex multistep process leading to malignant transformation by chemicals remain largely unknown. We have analysed changes in gene expression profiles in primary human hepatocytes and differentiated human hepatoma HepaRG cells after a 24 h treatment with 0.05 or 0.25µM aflatoxin B1 (AFB1), a potent genotoxic hepatocarcinogen. Three independent biological replicates of HepaRG cell cultures and two pools of three primary human hepatocyte cultures each, were investigated. Cells were treated with 0.05 or 0.25µM AFB1 for 24 h.

2010-12-07 | E-GEOD-25844 | biostudies-arrayexpress

Molecular Disruption and Dysfunction in the Thyroid of Rats Chronically Exposed to NaAsO2-Insights Unveiled through Proteomic and Phosphoproteomic Analyses

Project description:Arsenic, ubiquitously present as a hazardous metalloid, constitutes a significant danger to human health. Although investigations into the detrimental effects of arsenic on the thyroid have been initiated by researchers, a comprehensive exploration of its toxicological impact and underlying molecular mechanisms remains to be undertaken. In this study, we observed a cumulative effect of arsenic on the thyroid, identifying histological impairments and dysfunction in the thyroid of rats with chronic sodium arsenite (NaAsO2) exposure. These findings indicate that NaAsO2 induces significant thyroid damage. Subsequently, we employed proteomic and phosphoproteomic analyses to investigate the molecular mechanisms underlying the effects of chronic NaAsO2 exposure on the thyroid in rats. We observed that NaAsO2 disrupted the synthesis of thyroid hormones (THs), altered the expression level of THs synthesizing enzyme DUOX2. Additionally, Oxidative phosphorylation, AMPK signaling pathway, Central carbon metabolism in cancer, Cysteine and methionine metabolism, Cellular response to heat stress, and Protein processing in endoplasmic reticulum were upregulated, while Glutathione metabolism was downregulated. In conclusion, this study has unveiled the thyroid damage in rats induced by chronic NaAsO2 exposure and elucidated the disrupted molecular pathways, thereby providing novel insights into the molecular mechanisms underlying arsenic exposure and its impact on thyroid function.

2024-09-16 | PXD056135 |

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data