Substrate elasticity regulates vascular endothelial growth factor A (VEGFA) expression in adipose-derived stromal cells: Implications for potential angiogenesis.
Xie J., Zhang D., Ling Y., Yuan Q., Chenchen Z., Wei D.
Animal Study on Face & Skin, published in Colloids Surf B Biointerfaces (2018) — 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
- Animal Study
- Journal
- Colloids Surf B Biointerfaces (2018)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 30580148
- DOI
- 10.1016/j.colsurfb.2018.08.035
- Citations
- 11
Abstract (original English)
Adipose-derived stromal cells (ASCs) have potential in bioengineering angiogenesis due to their paracrine role in supporting endothelial tubulogenesis and vascular network formation. However, the precise mechanism of the inner angiogenic capacity of ASCs determined by the biophysical properties of the extracellular matrix needs to be further elucidated. In the current study, we fabricated two silicon-based elastomer polydimethylsiloxane (PDMS) substrates with different stiffnesses (stiff substrate, E = 195 kPa and soft substrate, E = 15 kPa) and found there were cytoskeletal changes in ASCs in response to different substrate stiffnesses. We then showed the expression of vinculin in focal adhesion plaques was enhanced and the nuclear translocation of β-catenin signaling was increased in ASCs on the stiff substrate relative to those on the soft substrate. We next used bioinformatics and found the downstream proteins of β-catenin signaling had binding sites in the promoter of vascular endothelial growth factor A (VEGFA), which is responsible for angiogenesis; then, we further confirmed the enhanced endogenous VEGFA expression in ASCs on the stiff substrate relative to that on the soft substrate. Finally, by using ectogenic VEGFA, we showed the stiff substrate could promote angiogenesis of ASCs in the form of more ring-like formations in 2D and vessel-like structure formations in 3
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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