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A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells (ChIP-Seq)

ABSTRACT: A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells (ChIP-Seq)

PROVIDER: PRJNA413404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6133362.fastq.gz	Fastqsanger.gz
	SRR6133363.fastq.gz	Fastqsanger.gz
	SRR6133364.fastq.gz	Fastqsanger.gz
	SRR6133365.fastq.gz	Fastqsanger.gz

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A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells (RNA-Seq)

Project description:Soon after release from stemness, a relevant portion of mouse embryonic stem cells (mES), kept in naïve state by MEK inhibitor, GSK3 inhibitor and LIF (2i/L), expresses endothelial nitric oxide synthase (eNOS) and endogenously synthesizes nitric oxide (NO). In this condition, an eNOS/NO-positive subpopulation (ESNO+) has been recognized by 4-amino-5-methylamino-2′,7′-difluorescein (DAF) fluorescence. Sorted ESNO+ cells expressed high levels of mesendodermal markers and efficiently generated cardiovascular precursors compared to eNOS/NO-negative cells (ESNO-). Mechanistically, the endogenous NO production deter- mined a rapid S-nitrosylation of Hdac2, a post-translational modification that compromised Hdac2 association with the transcription repression factor Zeb1. This condition destabilized Zeb1/chromatin interaction with genomic loci encoding for mesendodermal genes. Remarkably, Zeb1 or Hdac2 targeting activated an unscheduled transcription of mesendodermal lineage-associated genes in naïve mES revealing the Hdac2-Zeb1 pathway important for stemness maintenance in 2i/L. In contrast, eNOS targeting significantly reduced the endogenous NO production preventing the activation of mesendodermal gene transcription.

2018-10-31 | GSE104647 | GEO

A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells (ChIP-Seq)

2018-10-31 | GSE104646 | GEO

A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells

Project description:A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells

| PRJNA413397 | ENA

A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells (RNA-Seq)

Project description:A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells (RNA-Seq)

| PRJNA413403 | ENA

Zeb1-Hdac2-eNOS circuitry identifies early cardiovascular precursors in naive mouse embryonic stem cells.

Project description:Nitric oxide (NO) synthesis is a late event during differentiation of mouse embryonic stem cells (mESC) and occurs after release from serum and leukemia inhibitory factor (LIF). Here we show that after release from pluripotency, a subpopulation of mESC, kept in the naive state by 2i/LIF, expresses endothelial nitric oxide synthase (eNOS) and endogenously synthesizes NO. This eNOS/NO-positive subpopulation (ESNO+) expresses mesendodermal markers and is more efficient in the generation of cardiovascular precursors than eNOS/NO-negative cells. Mechanistically, production of endogenous NO triggers rapid Hdac2 S-nitrosylation, which reduces association of Hdac2 with the transcriptional repression factor Zeb1, allowing mesendodermal gene expression. In conclusion, our results suggest that the interaction between Zeb1, Hdac2, and eNOS is required for early mesendodermal differentiation of naive mESC.

| S-EPMC5876398 | biostudies-literature

A Zeb1 Hdac2 eNOS feedback circuitry identifies early cardiovascular precursors in naïve mouse embryonic stem cells

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

2018-10-31 | GSE104649 | GEO

eNOS interactors in human cells

Project description:Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of L-arginine and molecular oxygen into L-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease. Several mechanisms regulate eNOS activity and function, including phosphorylation at Ser and Thr residues and protein-protein interactions. Combining a tandem affinity purification approach and mass spectrometry, we identified stromal cell-derived factor 2 (SDF2) as a component of the eNOS macromolecular complex in endothelial cells. SDF2 knockdown impaired agonist stimulated NO synthesis and decreased phosphorylation of eNOS at Ser1177, a key event required for maximal activation of eNOS. Conversely, SDF2 overexpression dose-dependently increased NO synthesis through a mechanism involving Akt and calcium (induced with ionomycin), which increased the phosphorylation of Ser1177 in eNOS. NO synthesis by iNOS (inducible NOS) and nNOS (neuronal NOS) was also enhanced upon SDF2 overexpression. We found that SDF2 was a client protein of the chaperone protein Hsp90, interacting preferentially with the M domain of Hsp90, which is the same domain that binds to eNOS. In endothelial cells exposed to vascular endothelial growth factor (VEGF), SDF2 was required for the binding of Hsp90 and calmodulin to eNOS, resulting in eNOS phosphorylation and activation. Thus, our data describe a function for SDF2 as a component of the Hsp90-eNOS complex that is critical for signal transduction in endothelial cells.

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Gene expression for eNOS S1176 mutant mice

Project description:Extensive reports in the past decade have shown the importance of eNOS expression in atherogenesis. However, both the eNOS knockout and overexpression mouse models exhibit paradoxical results of increased atherosclerotic lesions. Our genetic approach herein utilizes endogenous point-mutations at the eNOS S1176 site to effectively manipulate eNOS activity rather than total eNOS protein expression levels. Our efforts definitively show that eNOS S1176 phosphorylation is sufficient to mitigate atherosclerotic lesion progression.

2023-11-10 | GSE243000 | GEO

Transcriptional profiling identifies white matter changes in eNOS+/- mice II

Project description:To elucidate the effects of Sodium nitrate feeding eNOS deficiency at the transcriptional level, RNA-seq was performed on white matter region dissected from the brains of eNOS+/+ and eNOS-/- and eNOS -/- + Sodium Nitrate treatment

2022-07-12 | GSE207960 | GEO

Transcriptional profiling identifies white matter changes in eNOS+/- mice I

Project description:To elucidate the effects of eNOS deficiency at the transcriptional level, we performed RNA-seq on white matter and grey matter regions dissected from the brains of eNOS+/+ and eNOS+/- mice

2022-07-12 | GSE207961 | GEO

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