ArticleLife science alliance2022
VEGFR3 modulates brain microvessel branching in a mouse model of 22q11.2 deletion syndrome.
Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- Article
- Tbx1 heterozygosity in the oligodendrocyte lineage shifts myelinated axon composition in the mouse fimbria without behavioral impairments.Molecular brain · 2026Article
- Distinct cellular and transcriptional mechanisms mediate an antioxidant therapeutic response in 22q11-deleted upper layer cortical projection neurons.bioRxiv : the preprint server for biology · 2025Article
- Pro-Angiogenic Bioactive Molecules in Vascular Morphogenesis: Integrating Endothelial Cell Dynamics.Current issues in molecular biology · 2025Review
- Unique Functional Neuroimaging Signatures of Genetic Versus Clinical High Risk for Psychosis.Biological psychiatry · 2025Article
- FLT4 causes developmental disorders of the cardiovascular and lymphovascular systems via pleiotropic molecular mechanisms.Cardiovascular research · 2024Article
- Involvement of an Aberrant Vascular System in Neurodevelopmental, Neuropsychiatric, and Neuro-Degenerative Diseases.Life (Basel, Switzerland) · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The loss of a single copy of <i>TBX1</i> accounts for most of the clinical signs and symptoms of 22q11.2 deletion syndrome, a common genetic disorder that is characterized by multiple congenital anomalies and brain-related clinical problems, some of which likely have vascular origins. <i>Tbx1</i> mutant mice have brain vascular anomalies, thus making them a useful model to gain insights into the human disease. Here, we found that the main morphogenetic function of TBX1 in the mouse brain is to suppress vessel branching morphogenesis through regulation of <i>Vegfr3</i> We demonstrate that inactivating <i>Vegfr3</i> in the <i>Tbx1</i> expression domain on a <i>Tbx1</i> mutant background enhances brain vessel branching and filopodia formation, whereas increasing <i>Vegfr3</i> expression in this domain fully rescued these phenotypes. Similar results were obtained using an in vitro model of endothelial tubulogenesis. Overall, the results of this study provide genetic evidence that <i>VEGFR3</i> is a regulator of early vessel branching and filopodia formation in the mouse brain and is a likely mediator of the brain vascular phenotype caused by <i>Tbx1</i> loss of function.
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