P86	Circulating progenitor cells fully preserve their migratory and proliferative response following acute myocardial infarction.
1S.Vöö, 2J.Eggermann, 1M.Dunaeva, 1J.Waltenberger
1Department of Cardiology, University of Maastricht/ Cardiovascular Research Institute of Maastricht, Maastricht, NL; 2Department of Internal Medicine II, Ulm University Medical Center, Ulm, DE.

Blood-derived CD133(+) circulating progenitor cells (CPC) were shown to contribute to the recovery of myocardial function following acute myocardial infarction (AMI). However, the nature of their underlying effects remains to be demonstrated. Localization to the ischemic area, transmigration through the endothelium and local survival are critical components in this scenario. Therefore, we analyzed transmigration and proliferation of CPC following AMI in comparison to control subjects in order to determine their functional integrity. CPC were isolated from 20 patients on day two after AMI following primary PCI (CKpeak 3288±1460 U/L) and from 25 control subjects (>6 month after successful PCI). CD133(+) CPC were isolated from peripheral blood using a positive selection (magnetic cell sorting) with a purity of >90%. Cell cycle phases were evaluated by flow cytometry and the migratory response of CPC upon stimulation with VEGF-A was assessed by a transmembrane chemotaxis assay. The transmigratory response of CPC towards VEGF-A was fully preserved on day two post-AMI (1.7-fold increase post-AMI versus 1.5-fold in controls). Likewise, the percentage of cells in S/M-phase was slightly increased in AMI (1.5±0.4%) versus controls (0.9±0.6%). Moreover, 90.7±0.6% and 95.1±1.8% of cells were in G0/G1-phase in AMI and controls, respectively. In the early post-AMI period, the transmigratory response of CPC towards VEGF is not impaired but even shows a tendency to increase in comparison to controls. Moreover, the level of CPC proliferation is slightly upregulated soon after AMI. These findings support the idea that AMI-associated conditions do not negatively affect CD133(+) CPC and might further support their beneficial contribution to cardiovascular repair.

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