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Transcriptional impacts of lipids on hESC

ABSTRACT: Transcriptional impacts of lipids on hESC

PROVIDER: PRJNA698483 | ENA |

REPOSITORIES: ENA

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Transcriptional impacts of lipids on hESC

Project description:Pluripotent stem cells can be maintained in a continuum of cellular states with distinct features. Exogenous lipid supplements are commonly utilized to shift the balance of global metabolism relieving the dependence on de novo lipogenesis. However, it is largely unexplored how specific lipid components regulate metabolism and pluripotency state. In this study, we investigate the impact of lipid supplements on human embryonic stem cells (hESCs), and report that signaling lipid lysophosphatidic acid (LPA) is the key component to shift the metabolic landscape in lipid supplement AlbuMAX. Although the maintenance of ERK phosphorylation and primed pluripotency is independent of exogenous lipids, LPA increases ERK phosphorylation, especially upon niche disintegration. We further demonstrate that LPA leads to distinctive transcriptome profile that is not associated with de novo lipogenesis. We also show that LPA causes unique and reversible phenotypes in cell cycle, morphology and mitochondria. This study reveals an LPA -induced primed state that allow people to drastically alter cell physiology for basic research and stem cell applications with hESCs.

2021-11-16 | GSE165892 | GEO

TMT characterisation: iPSC vs hESC

Project description:Detailed comparison of human pluripotent stem cells, to determine how hESC and iPSC differ in their protein expression profiles. The data was acquired in a TMT 10-plex SPS-MS3. 4 replicates of hESC compared to 4 replicates of HipSci human iPSCs.

2021-11-03 | PXD014502 | Pride

Tamoxifen transcriptional regulation in human endometrial stromal cells (HESC)

Project description:Tamoxifen transcriptional regulation in human endometrial stromal cells (HESC)

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transcriptional profiling of H9 human embronic stem cells (hESC) and hESC derived retinal pigment epithelium (RPE)

Project description:transcriptional profiling of H9 human embronic stem cells (hESC) and hESC derived retinal pigment epithelium (RPE)

| PRJNA524714 | ENA

transcriptional profiling of H9 human embronic stem cells (hESC) and hESC derived retinal pigment epithelium (RPE)

Project description:RPE was derived from hESC based on the protocol described in Zhu et al. PlosOne. 2013.

2020-02-28 | GSE127352 | GEO

Postnatal lipids drive hepatocyte maturation

Project description:Postnatal lipids drive hepatocyte maturation

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A post-transcriptional program coordinated by CSDE1 prevents intrinsic neural differentiation of human embryonic stem cells

Project description:While the transcriptional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little is known about how post-transcriptional modulations determine hESC function. RNA-binding proteins play central roles in RNA regulation, including translation and turnover. Here we show that the RNA-binding protein CSDE1 is highly expressed in hESCs to maintain their undifferentiated state and prevent default neural fate. Notably, loss of CSDE1 accelerates neural differentiation and potentiates neurogenesis. Conversely, ectopic expression of CSDE1 impairs neural differentiation. We find that CSDE1 post-transcriptionally modulates core components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis. Among these key pro-neural/neuronal factors, CSDE1 binds fatty acid binding protein 7 (FABP7) and vimentin (VIM) mRNAs as well as transcripts involved in neuron projection development regulating their stability and translation. Thus, our results uncover CSDE1 as a central post-transcriptional regulator of hESC identity and neurogenesis.

2018-05-16 | PXD007270 | Pride

nascent RNAseq of hESC.

Project description:nascent RNAseq of hESC.

| PRJEB15609 | ENA

A post-transcriptional program coordinated by CSDE1 prevents intrinsic neural differentiation of human embryonic stem cells

Project description:We compared hESCs with their neuronal counterpart to quantify differences in the expression of cold-shock domain containing proteins. While the transcriptional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little is known about how post-transcriptional modulations determine hESC function. RNA-binding proteins play central roles in RNA regulation, including translation and turnover. Here we show that the RNA-binding protein CSDE1 is highly expressed in hESCs to maintain their undifferentiated state and prevent default neural fate. Notably, loss of CSDE1 accelerates neural differentiation and potentiates neurogenesis. Conversely, ectopic expression of CSDE1 impairs neural differentiation. We find that CSDE1 post-transcriptionally modulates core components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis. Among these key pro-neural/neuronal factors, CSDE1 binds fatty acid binding protein 7 (FABP7) and vimentin (VIM) mRNAs as well as transcripts involved in neuron projection development regulating their stability and translation. Thus, our results uncover CSDE1 as a central post-transcriptional regulator of hESC identity and neurogenesis.

2018-05-16 | PXD007738 | Pride

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [targeted exome sequencing]

Project description:Human embryonic stem cells (hESC) and cancer cells rapidly divide with a short G1/S-phase causing increased replicative stress (RS). Since both in vitro cultured hESCs and most high-risk neuroblastomas have large chromosome 17q gains (17q+), we hypothesize that this may provide a "RS-resistance phenotype". We co-cultured parental cells and a derived hESC line with 17q+ under normal growth conditions and under RS. We could show a proliferative ad-vantage of hESC with 13q+17q+ over wild type by measurement of the cumulative growth and molecular analysis for chromosomal copy number analysis. To monitor effects of 17q+ on RS-resistance, cell cycle and transcriptome analysis were performed. In conclusion, we show that extra chromosomal aberrations, such as 17q+, provide proliferative advantage to hESC under RS and suggest that this phenomenon explains the high incidence of 17q+ in in vitro cultured hESC lines.

2021-05-11 | GSE155181 | GEO

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