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Chromatin structure profiling of Zeb1-knockdown mouse retina endothelial cells by ATAC-seq

ABSTRACT: Chromatin structure profiling of Zeb1-knockdown mouse retina endothelial cells by ATAC-seq

PROVIDER: PRJNA668146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12797026_1.fastq.gz	Fastqsanger.gz
	SRR12797026_2.fastq.gz	Fastqsanger.gz
	SRR12797027_1.fastq.gz	Fastqsanger.gz
	SRR12797027_2.fastq.gz	Fastqsanger.gz
	SRR12797028_1.fastq.gz	Fastqsanger.gz

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Chromatin structure profiling of Zeb1-knockdown mouse retina endothelial cells by ATAC-seq

Project description:By comparing ATAC-seq from freshly isolated endothelial cells from control or Zeb1-knockdown retina, we observed an increase in the accessibility of chromatin structure in endothelial cells after Zeb1-knockdown. We used ATAC-seq to study the functional role of Zeb1 and identified genes that exhibited increase of accessibilities to their transcription start sites (TSS).

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Transcriptome sequencing analysis of Zeb1-knockdown retina endothelial cells by RNA-seq

Project description:Transcriptome sequencing analysis of Zeb1-knockdown retina endothelial cells by RNA-seq

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Zeb1-knockdown retina endothelial cells

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Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

Project description:Endothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here we report that constitutive over-expression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell (EC) migration across the retinal surface and subsequent EC invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front, and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principle of angiogenesis. In the developing retina, Edn2 over-expression leads to over-production of endothelial tip cells by both morphologic and molecular criteria. Spatially localized over-expression of Edn2 produces a correspondingly localized endothelial response. Edn2 over-expression in the early embryo inhibits vascular development at mid-gestation, but Edn2 over-expression in developing skin and brain has no discernable effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A (Ednra) but not Ednrb in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it over-rides the activities of other homeostatic regulators of angiogenesis, such as vascular endothelial growth factor. Z/Edn2 females were crossed to Six3-Cre; Six3-Cre males. Postnatal P8 pups were genotyped for the Z/Edn2 allele by detection of Laz-Z activity in tail clips. Retinas from 2 - 3 pups were pooled for each data point.

2014-01-01 | E-GEOD-50059 | biostudies-arrayexpress

Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

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Project description:The zinc finger e-box binding homeobox 1 (ZEB1) transcription factor is a master regulator of the epithelial to mesenchymal transition (EMT), and of the reverse mesenchymal to epithelial transition (MET) processes. ZEB1 plays an integral role in mediating cell state transitions during cell lineage specification, wound healing and disease. EMT/MET are characterized by distinct changes in molecular and cellular phenotype that are generally context-independent. Posterior polymorphous corneal dystrophy (PPCD), associated with ZEB1 insufficiency, provides a new biological context in which to understand and evaluate the classic EMT/MET paradigm. PPCD is characterized by a cadherin-switch and transition to an epithelial-like transcriptomic and cellular phenotype, which we study in a cell-based model of PPCD generated using CRISPR-Cas9-mediated ZEB1 knockout in corneal endothelial cells (CEnCs). Transcriptomic and functional studies support the hypothesis that CEnC undergo an MET-like transition in PPCD, termed endothelial to epithelial transition (EnET), and lead to the conclusion that EnET may be considered a corollary to the classic EMT/MET paradigm.

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Expression data from Zeb1 knockdown NM18 cells

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