ArticleThe American journal of pathology2011
VEGFR-1 mediates endothelial differentiation and formation of blood vessels in a murine model of infantile hemangioma.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Infantile hemangiomas and retinopathy of prematurity: clues to the regulation of vasculogenesis.European journal of pediatrics · 2013Pooled it
- HDAC inhibition reprograms stem cell fate to suppress infantile hemangioma vasculogenesis.Angiogenesis · 2026Article
- VEGFA promotes odonto/osteoblastic differentiation in dental pulp stem cells via ERK/p38 signaling.Journal of dental sciences · 2025Article
- Immune-privileged cord blood-derived endothelial colony-forming cells: advancing immunomodulation and vascular regeneration.Angiogenesis · 2025Review
- An endothelial SOX18-mevalonate pathway axis enables repurposing of statins for infantile hemangioma.The Journal of clinical investigation · 2025Article
- Decoding infantile hemangioma: cellular dynamics, molecular signals, and microenvironmental influences.Frontiers in oncology · 2025Review
- Once a day administration of R(+) propranolol is sufficient to block vasculogenesis in a xenograft model of infantile hemangioma.Journal of vascular anomalies · 2024Article
- Infantile hemangioma: the common and enigmatic vascular tumor.The Journal of clinical investigation · 2024Review
- Global research trends of infantile hemangioma: A bibliometric and visualization analysis from 2000 to 2022.Heliyon · 2023Article
- Differential pericyte marker expression in craniofacial benign and malignant vascular tumors.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2023Article
- Nano-gold micelles loaded Dox and Elacridar for reversing drug resistance of breast cancer.IET nanobiotechnology · 2023Article
- CD146Frontiers in oncology · 2023Article
- Non-beta blocker enantiomers of propranolol and atenolol inhibit vasculogenesis in infantile hemangioma.The Journal of clinical investigation · 2022Article
- EndothelialArteriosclerosis, thrombosis, and vascular biology · 2022Article
- Current concepts on endothelial stem cells definition, location, and markers.Stem cells translational medicine · 2021Review
- The flavonoid luteolin suppresses infantile hemangioma by targeting FZD6 in the Wnt pathway.Investigational new drugs · 2021Article
- Peripheral vascular disease: preclinical models and emerging therapeutic targeting of the vascular endothelial growth factor ligand-receptor system.Expert opinion on therapeutic targets · 2021Review
- A data-driven computational model enables integrative and mechanistic characterization of dynamic macrophage polarization.iScience · 2021Article
- Giant Hepatic Hemangioma Regressed Significantly Without Surgical Management: A Case Report and Literature Review.Frontiers in medicine · 2021Article
- Oral atenolol treatment for infantile hemangiomas: clinical analysis of 133 consecutive patients.Annals of translational medicine · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Vascular endothelial growth factor receptor-1 (VEGFR-1) is a member of the VEGFR family, and binds to VEGF-A, VEGF-B, and placental growth factor. VEGFR-1 contributes to tumor growth and metastasis, but its role in the pathological formation of blood vessels is still poorly understood. Herein, we used infantile hemangioma (IH), the most common tumor of infancy, as a means to study VEGFR-1 activation in pathological vasculogenesis. IH arises from stem cells (HemSCs) that can form the three most prominent cell types in the tumor: endothelial cells, pericytes, and adipocytes. HemSCs can recapitulate the IH life cycle when injected in immuncompromised mice, and are targeted by corticosteroids, the traditional treatment for IH. We report here that VEGF-A or VEGF-B induces VEGFR-1-mediated ERK1/2 phosphorylation in HemSCs and promotes differentiation of HemSCs to endothelial cells. Studies of VEGFR-2 phosphorylation status and down-regulation of neuropilin-1 in the HemSCs demonstrate that VEGFR-2 and NRP1 are not needed for VEGF-A- or VEGF-B-induced ERK1/2 activation. U0216-mediated blockade of ERK1/2 phosphorylation or shRNA-mediated suppression of VEGFR-1 prevents HemSC-to-EC differentiation. Furthermore, the down-regulation of VEGFR-1 in the HemSCs results in decreased formation of blood vessels in vivo and reduced ERK1/2 activation. Thus, our study reveals a critical role for VEGFR-1 in the HemSC-to-EC differentiation that underpins pathological vasculogenesis in IH.
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