The JAK/STAT3 signalling pathway regulated angiogenesis in an endothelial cell/adipose-derived stromal cell co-culture, 3D gel model.
Xue C., Xie J., Zhao D., Lin S., Zhou T., Shi S.
Animal Study, published in Cell Prolif (2016) — 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
- Cell Prolif (2016)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 27667148
- PMCID
- PMC6529085
- DOI
- 10.1111/cpr.12307
- Citations
- 73
Abstract (original English)
Objectives The aim of the study was to investigate the role of the JAK/STAT3 signalling pathway in angiogenesis. Materials and methods The model established in vitro, involved a 3D collagen gel being implanted with endothelial cells (ECs) from red fluorescent protein-labelled mice, and adipose-derived stromal cells (ASCs) from green fluorescent protein-labelled mice. Phenomena of angiogenesis, after treatment by the inhibitor and the activator of JAK/STAT3 pathway respectively, were observed using confocal laser scanning microscopy. Transwell co-culture of ECs and ASCs was used to elucidate mechanisms. Results Stattic, inhibitor of JAK/STAT3 pathway, attenuated angiogenesis in the model. In contrast, angiogenesis was promoted after treatment of Olanzapine, an activator. We found that protein levels of VEGFA and cyclin D1 were regulated by the JAK/STAT3 pathway, and flow cytometry further confirmed variations in cell cycle parameters of ECs and ASCs. Genes VEGFA/B, VEGFR2, MMP-2, MMP-9, IGF-1 and b-FGF were down-regulated by Stattic in ECs, while Olanzapine significantly up-regulated mRNA levels of these genes. As for ASCs, genes VEGFA, MMP-2, MMP-9, IGF-1 and b-FGF were modulated by the JAK/STAT3 pathway. Conclusions Angiogenesis in the 3D collagen gel was regulated by the JAK/STAT3 pathway which involved changes in vessel length, vessel diameter and sprout number. The underlyi
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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