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Specialized endothelial tip cells guide neuroretina vascularization and blood-retina-barrier formation

ABSTRACT: Specialized endothelial tip cells guide neuroretina vascularization and blood-retina-barrier formation

PROVIDER: PRJNA734268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14699800.fastq.gz	Fastqsanger.gz
	SRR14699801.fastq.gz	Fastqsanger.gz
	SRR14699802.fastq.gz	Fastqsanger.gz
	SRR14699803.fastq.gz	Fastqsanger.gz
	SRR14699804.fastq.gz	Fastqsanger.gz

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Similar Datasets

Specialized endothelial tip cells guide neuroretina vascularization and blood-retina-barrier formation

Project description:Endothelial tip cells guiding tissue vascularization are primary targets for angiogenic therapies. Whether tip cells require differential signals to develop their complex branching patterns remained unknown. Here we show that diving tip cells invading the neuroretina (D-tip cells) are distinct from tip cells guiding the superficial retinal vascular plexus (S-tip cells). D-tip cells have a unique transcriptional signature, including high TGFβ signaling, and acquire blood-retina barrier properties. Endothelial deletion of TGFβ receptor I (Alk5) inhibits D-tip cell identity acquisition and deep vascular plexus formation. Loss of endothelial ALK5, but not of the canonical SMAD effectors, leads to aberrant contractile pericyte differentiation, and hemorrhagic vascular malformations. Our data reveal stage-specific tip cell heterogeneity as a requirement for retinal vascular development and suggest that noncanonical-TGFβ signaling could improve retinal revascularization and neural function in ischemic retinopathy.

2021-07-16 | GSE175895 | GEO

Specialized endothelial tip cells guide neuroretina vascularization and blood-retina-barrier formation.

Project description:Endothelial tip cells guiding tissue vascularization are primary targets for angiogenic therapies. Whether tip cells require differential signals to develop their complex branching patterns remained unknown. Here, we show that diving tip cells invading the mouse neuroretina (D-tip cells) are distinct from tip cells guiding the superficial retinal vascular plexus (S-tip cells). D-tip cells have a unique transcriptional signature, including high TGF-β signaling, and they begin to acquire blood-retina barrier properties. Endothelial deletion of TGF-β receptor I (Alk5) inhibits D-tip cell identity acquisition and deep vascular plexus formation. Loss of endothelial ALK5, but not of the canonical SMAD effectors, leads to aberrant contractile pericyte differentiation and hemorrhagic vascular malformations. Oxygen-induced retinopathy vasculature exhibits S-like tip cells, and Alk5 deletion impedes retina revascularization. Our data reveal stage-specific tip cell heterogeneity as a requirement for retinal vascular development and suggest that non-canonical-TGF-β signaling could improve retinal revascularization and neural function in ischemic retinopathy.

| S-EPMC9951594 | biostudies-literature

Microarray Analysis of Retinal Endothelial Tip Cells Identifies CXCR4 as a Mediator of Tip Cell Morphology and Branching

Project description:The development of the vertebrate vascular system is mediated by both genetic patterning of vessels and by angiogenic sprouting in response to hypoxia. Both of these processes depend on the detection of environmental guidance cues by endothelial cells. A specialized subtype of endothelial cell known as the tip cell is believed to be involved in the detection and response to these cues, but the molecular signaling pathways utilized by tip cells to mediate tissue vascularization remain largely uncharacterized. To identify genes critical to tip cell function, we have developed a method to isolate them using laser capture microdissection, permitting comparison of RNA extracted from endothelial tip cells to that of endothelial stalk cells using microarray analysis. Genes enriched in tip cells include ESM-1, Angiopoietin-2, and SLP-76. CXCR4, a receptor for the chemokine SDF-1, was also identified as a tip cell-enriched gene, and we provide evidence for a novel role for this receptor in mediating tip cell morphology and vascular patterning in the neonatal retina.

2010-03-17 | GSE19284 | GEO

Transcriptome gene expression analysis of root tip, leaf tip, shoot tip, root (without root tip) and leaf (without leaf tip) from Ceratopteris richardii sporophytes

Project description:To study genes specially expressed in root tip, leaf tip, shoot tip, root (without root tip) and leaf (without leaf tip) of Ceratopteris richardii, we carried out an RNA-seq to analyze gene expression levels from these five tissues.

2019-10-22 | GSE139160 | GEO

Transcriptome gene expression analysis of root tip, leaf tip, shoot tip, root (without root tip) and leaf (without leaf tip) from Ceratopteris richardii sporophytes

Project description:Transcriptome gene expression analysis of root tip, leaf tip, shoot tip, root (without root tip) and leaf (without leaf tip) from Ceratopteris richardii sporophytes

| PRJNA578676 | ENA

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.

2014-01-01 | GSE50059 | GEO

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

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

Failure of digit tip regeneration in the absence of Lmx1b suggests Lmx1b functions disparate from dorsoventral polarity

Project description:Mammalian digit tip regeneration is linked to the presence of nail tissue, but a nail-explicit model is missing. Here, we report that nail-less double-ventral digits of ΔLARM1/2 mutants that lack limb-specific Lmx1b enhancers, fail to regenerate. To separate the nail’s effect from the lack of DV polarity, we also interrogate double-dorsal double-nail digits and show that they regenerate. Thus, DV polarity is not a prerequisite for regeneration and the nail requirement is supported. Transcriptomic comparison between wild-type and non-regenerative ΔLARM1/2 mutant blastemas reveals differential up-regulation of vascularization and connective tissue functional signatures in wild-type versus upregulation of inflammation in the mutant. These results, together with the finding of Lmx1b expression in the postnatal dorsal dermis underneath the nail and uniformly in the regenerative blastema opens the possibility of additional Lmx1b roles in the progression of digit tip regeneration, in addition to the indirect effect of mediating the formation of the nail.

2022-12-02 | GSE202223 | GEO

root tip metagenome

Project description:Pinus radiata - root tip ITS sequencing

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High throughput single cell epigenomic profiling by targeted insertion of promoters (TIP-seq)

Project description:Chromatin profiling in single cells has been extremely challenging and almost exclusively limited to histone proteins. In cases where single cell methods have shown promise, many require highly specialized equipment or cell type specific protocols and are relatively low throughput. Here, we combine the advantages of tagmentation, linear amplification and combinatorial indexing to produce a high throughput single cell DNA binding site mapping method that is simple, inexpensive and capable of multiplexing several independent samples per experiment. Targeted Insertion of Promoters (TIP-seq) uses Tn5 fused to protein A to insert a T7 RNA polymerase promoter adjacent to a chromatin protein of interest. Linear amplification of flanking DNA with T7 polymerase prior to sequencing library preparation provides ~10-fold higher unique reads per single cell compared to other methods. We apply TIP-seq to map histone modifications, RNA Polymerase II (RNAPII) and transcription factor CTCF binding sites in single human and mouse cells.

2021-11-10 | GSE188512 | GEO

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