ArticlePloS one2015
TBX1 Represses Vegfr2 Gene Expression and Enhances the Cardiac Fate of VEGFR2+ Cells.
Article in PloS one, 2015. 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, 12 citations in OpenAlex.
- Identification and validation of biomarkers related to mitochondria-associated endoplasmic reticulum membranes in type 2 diabetes mellitus using peripheral blood transcriptomics.European journal of medical research · 2025Article
- Charting the Path: Navigating Embryonic Development to Potentially Safeguard against Congenital Heart Defects.Journal of personalized medicine · 2023Review
- VEGFR3 modulates brain microvessel branching in a mouse model of 22q11.2 deletion syndrome.Life science alliance · 2022Article
- Rare variants in KDR, encoding VEGF Receptor 2, are associated with tetralogy of Fallot.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Biochemical and Conformational Characterization of Recombinant VEGFR2 Domain 7.Molecular biotechnology · 2019Article
- Human Recombinant VEGFR2D4 Biochemical Characterization to Investigate Novel Anti-VEGFR2D4 Antibodies for Allosteric Targeting of VEGFR2.Molecular biotechnology · 2019Article
- Hedgehog Pathway Drives Fusion-Negative Rhabdomyosarcoma Initiated From Non-myogenic Endothelial Progenitors.Cancer cell · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The T-box transcription factor TBX1 has critical roles in maintaining proliferation and inhibiting differentiation of cardiac progenitor cells of the second heart field (SHF). Haploinsufficiency of the gene that encodes it is a cause of congenital heart disease. Here, we developed an embryonic stem (ES) cell-based model in which Tbx1 expression can be modulated by tetracycline. Using this model, we found that TBX1 down regulates the expression of VEGFR2, and we confirmed this finding in vivo during embryonic development. In addition, we found a Vegfr2 domain of expression, not previously described, in the posterior SHF and this expression is extended by loss of Tbx1. VEGFR2 has been previously described as a marker of a subpopulation of cardiac progenitors. Clonal analysis of ES-derived VEGFR2+ cells indicated that 12.5% of clones expressed three markers of cardiac lineage (cardiomyocyte, smooth muscle and endothelium). However, a pulse of Tbx1 expression was sufficient to increase the percentage to 20.8%. In addition, the percentage of clones expressing markers of multiple cardiac lineages increased from 41.6% to 79.1% after Tbx1 pulse. These results suggest that TBX1 plays a role in maintaining a progenitor state in VEGFR2+ cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.