Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Localized T3 production modifies the transcriptome and promotes the hepatocyte-like lineage in iPSC-derived hepatic organoidslineage in iPSC-derived hepatic organoids

ABSTRACT: Localized T3 production modifies the transcriptome and promotes the hepatocyte-like lineage in iPSC-derived hepatic organoidslineage in iPSC-derived hepatic organoids

PROVIDER: PRJNA1027474 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26372177_1.fastq.gz	Fastqsanger.gz
	SRR26372177_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Localized T3 production modifies the transcriptome and promotes the hepatocyte-like lineage in iPSC-derived hepatic organoidslineage in iPSC-derived hepatic organoids

Project description:Thyroid hormone (TH) levels are low during development, and the deiodinases control TH signaling through tissue-specific activation or inactivation of TH. Here we studied human iPSC-derived hepatic organoids and identified a robust induction in DIO2 expression (the deiodinase that activates T4 to T3) that occurs in hepatoblasts. The surge in D2-T3 persists until the hepatoblasts differentiate into hepatocytes- or cholangiocytes-like cells, neither of which express DIO2. Preventing the induction of the D2-T3 signaling modified the expression of key transcription factors, decreased the number of hepatocyte-like cells by ~60%, and increased the number of cholangiocyte-like cells by ~55% without affecting the growth or the size of the mature liver organoid. Physiological levels of T3 could not fully restore the transition from hepatoblasts to mature cells. This indicates that the timed surge in D2-T3 signaling critically determines the fate of developing human hepatoblasts and the transcriptome of the maturing hepatocytes, with physiological and clinical implications for how the liver handles energy substrates.

2024-01-24 | GSE245250 | GEO

Maturation of iPSC-derived Hepatocyte-Like Cells with 5 nM T3

Project description:Thyroid hormones are important for many developmental processes. We evaluated the improvement of iPSC-derived hepatocyte-like cell maturation under hypoxic culture conditions, specialized cell culture media, and ±5 nM T3 during the final week of culture in two iPSC lines.

2025-07-31 | E-MTAB-14973 | biostudies-arrayexpress

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

Maturation of iPSC-derived Hepatocyte-Like Cells with 5 nM T3

Project description:Maturation of iPSC-derived Hepatocyte-Like Cells with 5 nM T3

| PRJEB87645 | ENA

Localized T3 production modifies the transcriptome and promotes the hepatocyte-like lineage in iPSC-derived hepatic organoids.

Project description: Not available

| S-EPMC10795825 | biostudies-literature

Whole transcriptome analysis of iPSC derived hepatic organoids cultures

Project description:Whole transcriptome analysis of iPSC derived hepatic organoids cultures

| PRJNA576358 | ENA

Neonatal Thyroxine Activation Modifies Epigenetic Programming Of The Liver [ChIP-Seq]

Project description:In the neonatal liver, a peak of type 2 deiodinase (D2) activity accelerates local T3 production and the expression of thyroid hormone (TH)-responsive genes. Here we show that this acute increase in T3 signaling permanently modifies hepatic gene expression. Liver-specific Dio2 inactivation (Alb-D2KO) transiently increased H3K9me3 levels during post-natal days 1-5 (P1-P5) in discrete chromatin areas, and methylation of 1,508 DNA sites (H-sites) that remained in the adult mouse liver. These sites were associated with 1,551 areas of reduced chromatin accessibility (RCA; Atac-seq) within core promoters and 2,426 within intergenic regions, with reduction in the expression of 1,525 genes (RNA-seq). There was strong correlation between H-sites and RCA sites (r=0.85; p<0.0002), suggesting a cause-effect relationship. The analysis of chromosome conformation capture (Hi-C) data revealed a set of 57 repressed genes that have a promoter RCA in close contact with an intergenic RCA ~300 Kbp apart, including Foxa2 that plays an important role during development. Thus, the post-natal surge in hepatic D2 activity and TH-signaling prevents discrete DNA methylation and modifies the transcriptome of the adult mouse. This explains how the systemic T3 hormone acts locally during development to define future chromatin accessibility and expression of critically relevant hepatic genes.

2021-06-18 | GSE162887 | GEO

Neonatal Thyroxine Activation Modifies Epigenetic Programming Of The Liver [RNA-Seq]

2021-06-18 | GSE162890 | GEO

Neonatal Thyroxine Activation Modifies Epigenetic Programming Of The Liver [ATAC-Seq]

2021-06-18 | GSE162929 | GEO

sibling aHDF-iPSC clones derived from the same fibroblasts

Project description:Hepatocytes generated from human induced pluripotent stem cells (hiPSCs) are unprecedented resources for pharmaceuticals and cell therapy. However, little attention has so far been paid to variations among hiPSC lines in terms of their hepatic differentiation. We developed an improved hepatic differentiation protocol and compared multiple hiPSC lines. This comparison indicated that the hepatic differentiation propensity varies among sibling hiPSC clones derived from the same adult human dermal fibroblasts (aHDFs). In addition, hiPSC clones derived from peripheral blood cells (PB-iPSCs) consistently showed good hepatic differentiation efficiency, whereas many hiPSC clones from adult dermal fibroblasts (aHDF-iPSCs) showed poor hepatic differentiation. However, when we compared hiPSCs from blood and dermal fibroblasts from the same individuals, we found that variations in hepatic differentiation were largely attributable to donor differences, rather than to the types of the original cells. In order to understand the molecular mechanisms underlying the observed variations in hepatic differentiation, we performed microarray analyses of sibling aHDF-iPSC clones, and aHDF- and PB-iPSC clones from the same individuals. sibling aHDF-iPSC clones (201B6 and 201B7; derived from the same aHDFs) (1) undifferentiated state (n=4, biological replicate #1-#4) (2) CXCR4-positive cell populations sorted by flowcytometry after 7 days of endodermal differentiation (n=4, biological replicate #1-#4) (3) CXCR4-negative cell populations sorted by flowcytometry after 7 days of endodermal differentiation (n=4, biological replicate #1-#4)

2012-07-15 | E-GEOD-38152 | biostudies-arrayexpress

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