The authors compared the endothelial differentiation capacities of human and rat adipose-derived stem cells to determine whether human adipose-derived stem cells can be a source of endothelial cells clinically.
Human and rat adipose-derived stem cells were harvested and characterized with flow cytometry and trilineage differentiation. Cells from passages III through V were fed with endothelial cell differentiation medium for up to 3 weeks. Cells were harvested after 1, 2, and 3 weeks, and endothelial differentiation was evaluated with quantitative reverse-transcriptase polymerase chain reaction, flow cytometry, and angiogenic sprouting assays.
Both human and rat adipose-derived stem cells were CD90+, CD44+, and CD31− before differentiation. The cells were successfully differentiated into adipogenic, osteogenic, and chondrogenic lineages. Expression of endothelial cell–specific genes peaked at the second week of differentiation in both human and rat cells. The fold changes in expression of CD31, vascular endothelial growth factor receptor-1, nitric oxide synthase, and von Willebrand factor genes at week 2 were 0.4 ± 0.1, 34.7 ± 0.3, 2.03 ± 0.25, and 12.5 ± 0.3 respectively, in human adipose-derived stem cells; and 1.5 ± 1.01, 21.6 ± 1.7, 17.9 ± 0.6, and 11.2 ± 1.3, respectively, in rat cells. The percentages of CD31+ cells were 0.2, 0.64, and 1.6 in human cell populations and 0.5, 5.91, and 11.5 in rat cell populations at weeks 1, 2, and 3, respectively. Rat adipose-derived stem cell–derived endothelial cells displayed enhanced sprouting capability compared with the human cells.
Human adipose-derived stem cells responded less strongly to EGM-2MV endothelial differentiation medium than did the rat cells. Still, the human cells have the potential to become a clinical source of endothelial cells with modifications in the differentiation conditions.
Sacramento and Davis, Calif.
From the Department of Surgery, Division of Plastic Surgery, University of California, Davis Medical Center; and the Department of Biomedical Engineering, University of California, Davis.
Received for publication January 6, 2016; accepted July 25, 2016.
The first two authors contributed equally to this work.
Disclosure:The authors have no financial interest to declare in relation to the content of this article.
Supplemental digital content is available for this article. A direct URL citation appears in the text; simply type the URL address into any Web browser to access this content. A clickable link to the material is provided in the HTML text of this article on the Journal’s website (www.PRSJournal.com).
David E. Sahar, M.D., Department of Surgery, Division of Plastic Surgery, University of California, Davis Medical Center, 4625 2nd Avenue, Room 3001, Sacramento, Calif. 95817, email@example.com