ArticleStem cells translational medicine2022
Dll4 Inhibition Promotes Graft Retention in Fat Grafting Enriched with Adipose-Derived Stem Cells.
Article in Stem cells translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Modulating endothelial cell dynamics in fat grafting: the impact of DLL4 siRNA via adipose stem cell extracellular vesicles.American journal of physiology. Cell physiology · 2024Article
- Global Analyses and Latest Research Hot Spots of Adipose-Derived Stem Cells in Fat Grafting: A Bibliometric and Visualized Review.Aesthetic plastic surgery · 2023Review
- The Evolving Function of Vasculature and Pro-angiogenic Therapy in Fat Grafting.Cell transplantationReview
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autologous fat grafting is among the safest and most effective treatments for soft-tissue restoration and augmentation, and many efforts have been made to improve its efficiency, including adipose-derived stem cell (ASC) supplementation. Here, we investigated the role of Notch ligand Delta-like ligand 4 (Dll4) in angiogenesis within grafted fat and its effect on graft retention, as well as the effect of Dll4 inhibition on ASC supplementation. Using a murine fat graft model, we investigated the expression of Dll4 in fat grafts and assessed the graft volume, vascularity, and perfusion within the graft, and ASC differentiation patterns depending on the blockade of Dll4. The underlying mechanism of Dll4 inhibition on ASC supplemented fat grafts was investigated using transcriptome analysis. Dll4 was highly expressed in vascular endothelial cells (ECs) within grafted fat, where Dll4-blocking antibody treatment-induced angiogenesis, promoting fat graft retention. In addition, its effect on fat graft retention was synergistically improved when ASCs were concomitantly supplemented. The expression of junctional proteins was increased in ECs, and inflammatory processes were downregulated in grafted fat upon ASC supplementation and Dll4 inhibition. Dll4 inhibition induced vascularization within the grafted fat, thereby promoting graft retention and exhibiting synergistic effects with concomitant ASC supplementation. This study serves as a basis for developing new potential therapeutic approaches targeting Dll4 to improve graft retention after cell-assisted transfer.
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