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Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE212524 | GEO | 2024/08/18

REPOSITORIES: GEO

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Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [02RNF20_Huvec]

Project description:Tight control of cell fate choices is crucial for proper vessel development. Here we show that Rnf20, the major E3 ubiquitin ligase of histone H2B, plays a key role in the tight control of VEGF-Notch signaling, which is crucial for proper vessel growth and patterning, as well as for the dynamic tip-stalk cell fate at the vascular front. We demonstrate that Rnf20 is dynamically expressed in the developing retina and controls vessel growth through two distinct modes of action. On the one hand, it restricts gene activation by the endothelial transcription factor ERG and on the other, it orchestrates large-scale mRNA processing events, which change the bioavailability and function of critical pro-angiogenic factors. We show that Rnf20 plays a key role for the upregulation of both VEGFR2 through alternative polyadenylation and VEGFA through intron inclusion, as well as for suppressing the ability of Notch1 to bind to chromatin. Interestingly, perturbations of RNF20 have been associated with complex cardiovascular malformations in human patients, suggesting that delineating the mechanisms that control Rnf20 expression and activity may provide new insights into diseases caused by vascular dysfunction.

2024-08-18 | GSE212522 | GEO

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [Rnf20_CD31_RNA_seq]

2024-08-18 | GSE212520 | GEO

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [ChIP-seq]

2024-08-18 | GSE225943 | GEO

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [03ATAC_seq-Retina]

2024-08-18 | GSE212523 | GEO

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis

Project description:Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis

| PRJNA875892 | ENA

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [Rnf20_CD31_RNA_seq]

Project description:Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [Rnf20_CD31_RNA_seq]

| PRJNA875896 | ENA

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [02RNF20_Huvec]

Project description:Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [02RNF20_Huvec]

| PRJNA875898 | ENA

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [03ATAC_seq-Retina]

Project description:Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [03ATAC_seq-Retina]

| PRJNA875897 | ENA

Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [ChIP-seq]

Project description:Rnf20 levels modulate the VEGF-Notch signaling circuits during sprouting angiogenesis [ChIP-seq]

| PRJNA938058 | ENA

EphrinB2/EphB4 signaling regulates non-sprouting angiogenesis by VEGF.

Project description:Vascular endothelial growth factor (VEGF) is the master regulator of angiogenesis, whose best-understood mechanism is sprouting. However, therapeutic VEGF delivery to ischemic muscle induces angiogenesis by the alternative process of intussusception, or vascular splitting, whose molecular regulation is essentially unknown. Here, we identify ephrinB2/EphB4 signaling as a key regulator of intussusceptive angiogenesis and its outcome under therapeutically relevant conditions. EphB4 signaling fine-tunes the degree of endothelial proliferation induced by specific VEGF doses during the initial stage of circumferential enlargement of vessels, thereby limiting their size and subsequently enabling successful splitting into normal capillary networks. Mechanistically, EphB4 neither inhibits VEGF-R2 activation by VEGF nor its internalization, but it modulates VEGF-R2 downstream signaling through phospho-ERK1/2. In vivo inhibitor experiments show that ERK1/2 activity is required for EphB4 regulation of VEGF-induced intussusceptive angiogenesis. Lastly, after clinically relevant VEGF gene delivery with adenoviral vectors, pharmacological stimulation of EphB4 normalizes dysfunctional vascular growth in both normoxic and ischemic muscle. These results identify EphB4 as a druggable target to modulate the outcome of VEGF gene delivery and support further investigation of its therapeutic potential.

| S-EPMC5934775 | biostudies-literature

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