Key result
Allogeneic mesenchymal stem cell transplantation significantly increased capillary density in viable myocardium adjacent to the infarction compared to control in an ischaemic swine model (p=0.002).
Why the study?
Does allogeneic mesenchymal stem cell transplantation elicit neo-angiogenesis in an ischaemic swine model?
Does allogeneic mesenchymal stem cell transplantation elicit neo-angiogenesis in an ischaemic swine model?
p-value: p=0.002
Allogeneic mesenchymal stem cell transplantation enhances angiogenesis in viable myocardium adjacent to infarction in an ischaemic swine model without eliciting a specific cellular immune response when combined with short-term tacrolimus.
May support post-infarct angiogenesis research; leaves open translation to human therapy.
OBJECTIVES: Autologous mesenchymal stem cell transplantation has been shown to improve myocardial function in ischaemic cardiomyopathy. We studied one hypothetical mechanism, neo-angiogenesis, using allogeneic mesenchymal stem cell transplantation in an ischaemic swine model. METHODS: Allogeneic mesenchymal stem cells were injected in the peri-infarct area (1×10(6) cells kg(-1)) 2 weeks after myocardial infarction. Myocardial infarction alone (n=3) served as a control group. In the myocardial infarction-mesenchymal stem cells group (n=6), tacrolimus was given from day 0 to day 12. Capillary density and inflammatory/rejection processes (anti-factor VIII and anti-CD3/CD68 monoclonal antibodies, respectively) were compared between groups. RESULTS: In scarred myocardium, capillary density was similar between both ischaemic groups: 15.4 (±15.3) and 14.7 (±15.2) vessel/field in myocardial infarction-mesenchymal stem cells and myocardial infarction-alone groups (non-significant). In viable myocardium adjacent to the infarction, capillary density was significantly increased in the myocardial infarction-mesenchymal stem cells group than in the myocardial infarction-alone group (p=0.002). The number of infiltrating CD3+ cells was equivalent in both myocardial infarction-alone and myocardial infarction-mesenchymal stem cells groups (CD3+: 8.6% vs 9.3%, non-significant). However, CD68+ cell infiltration was more prominent after mesenchymal stem cell transplantation (4.7% vs 2% in myocardial infarction alone, p<0.01). CONCLUSIONS: Allogeneic mesenchymal stem cell transplantation enhances angiogenesis after myocardial infarction. This effect is limited to the viable myocardium. Using a concomitant 12-day course of tacrolimus, no mesenchymal stem cell-specific cellular immune response was demonstrated.
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Poncelet et al. (2010) studied Myocardial infarction (n=9). Allogeneic mesenchymal stem cell transplantation vs. Myocardial infarction alone was evaluated on Capillary density in viable myocardium adjacent to the infarction (p=0.002). Allogeneic mesenchymal stem cell transplantation significantly increased capillary density in viable myocardium adjacent to the infarction compared to control in an ischaemic swine model (p=0.002).
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