A human endothelial and adipose stem cell-based co-culture model for venous malformations.
Ansarizadeh M., Lazovic B., Sarmadian Z., Singh A., Hicks R., Eklund L.
Laboratory Study, published in Angiogenesis (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Angiogenesis (2026)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42070175
- PMCID
- PMC13136223
- DOI
- 10.1007/s10456-026-10045-9
Abstract (original English)
Venous malformations (VMs) are developmental defects in vascular morphogenesis characterized by enlarged vein-like channels and defective perivascular cell coverage. The majority of VMs are caused by somatic mutations in endothelial cell (EC) receptor tyrosine kinase TIE2, but current medicinal options are limited. The common bottleneck when testing new therapeutic strategies and identifying efficient drug candidates is the absence of a reliable and robust model for replicating the characteristics of VMs. We report here on an advanced in vitro model for recapitulating cellular and molecular pathologies of the VM-causative TIE2L914F mutation by co-culturing human adipose tissue-derived stem cells (hASCs) with either human umbilical vein ECs (HUVECs) retrovirally transduced to express TIE2L914F or with induced pluripotent stem cell-derived ECs (iECs) with locus-targeted TIE2L914F. For comparison, cellular and molecular crosstalk between vascular cell types was investigated in HUVEC and primary vascular smooth muscle cell (vSMC) co-cultures. Advanced microscopy and transcriptomic analysis were used to investigate the cellular and molecular phenotypes in vascular cell types. Comparison of TIE2WT, gain- (TIE2L914F) and loss-of-function mutations (TIE2KO) revealed the importance of TIE2 signaling for vascular network formation in hASC/EC co-cultures. The model recapitulated the cellu
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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