| Autor: |
Naaijkens BA; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands. paj.krijnen@vumc.nl.; Interuniversity Cardiology Institute of the Netherlands (ICIN), Utrecht, Netherlands. paj.krijnen@vumc.nl.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands. paj.krijnen@vumc.nl., Krijnen PA; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands., Meinster E; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands., ter Horst EN; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands.; Interuniversity Cardiology Institute of the Netherlands (ICIN), Utrecht, Netherlands.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands., Vo K; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands., Musters RJ; Department of Physiology, VU University Medical Center, Amsterdam, Netherlands.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands., Kamp O; Department of Cardiology, VU University Medical Center, Amsterdam, Netherlands.; Interuniversity Cardiology Institute of the Netherlands (ICIN), Utrecht, Netherlands., Niessen HW; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands.; Department of Cardiac Surgery, VU University Medical Center, Amsterdam, Netherlands.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands., Juffermans LJ; Department of Physiology, VU University Medical Center, Amsterdam, Netherlands.; Department of Cardiology, VU University Medical Center, Amsterdam, Netherlands.; Interuniversity Cardiology Institute of the Netherlands (ICIN), Utrecht, Netherlands.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands., van Dijk A; Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, Netherlands.; Institute of Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, Netherlands. |
| Abstrakt: |
In most pre-clinical animal studies investigating stem cell therapy in acute myocardial infarction (AMI), the administered stem cells are isolated from healthy donors. In clinical practice, however, patients who suffer from AMI will receive autologous cells, for example using adipose-derived stem cells (ASC). During AMI, inflammation is induced and we hypothesized that this might affect characteristics of ASC. To investigate this, ASC were isolated from rat adipose tissue 1 day (1D group, n = 5) or 7 days (7D group, n = 6) post-AMI, and were compared with ASC from healthy control rats (Control group, n = 6) and sham-operated rats (Sham 1D group, n = 5). We found that significantly fewer ASC were present 1 day post-AMI in the stromal vascular fraction (SVF), determined by a colony-forming-unit assay (p < 0.001 vs. Control and 7D). These data were confirmed by flow cytometry, showing fewer CD90-positive cells in SVF of the 1D group. When cultured, no differences were found in proliferation rate and cell size between the groups in the first three passages. Also, no difference in the differentiation capacity of ASC was found. In conclusion, it was shown that significantly fewer stem cells were present in the SVF 1 day post-AMI; however, the stem cells that were present showed no functional differences. |
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