期刊
JOURNAL OF INTERNAL MEDICINE
卷 265, 期 2, 页码 238-249出版社
WILEY
DOI: 10.1111/j.1365-2796.2008.02011.x
关键词
acute myocardial infarction; CD133; coronary heart disease; diabetes mellitus; progenitor cells
资金
- Deutsche Forschungsgemeinschaft (Heisenberg Scholarship) [WA 734/5-1]
- European Commission [504743]
- University of Maastricht/Cardiovascular Research Institute of Maastricht
Circulating progenitor cells (PC) can positively influence the healing of ischaemic myocardium. Cardiovascular risk factors including diabetes mellitus (DM) may have a negative influence on both number and recruitment of PC. Recent evidence suggests that less differentiated CD133(+)PC contribute to myocardial healing and are promising candidates for therapy. Therefore, we investigated whether DM affects CD133(+)PC. CD133(+)PC were analyzed in patients following acute myocardial infarction and successful reperfusion [acute myocardial infarction (AMI, n = 45) with/without non-insulin-requiring type 2 DM (T2DM)]. Stable coronary artery disease patients (CAD, n = 45) served as stable controls. Number and phenotype of CD133(+)PC were assessed by flow cytometry. CD133(+)PC chemotaxis was assessed towards vascular endothelial growth factor, an angiogenic stimulus upregulated in AMI. The expression of anti-oxidant enzymes in CD133(+)PC was detected by reverse-transcriptase PCR. In non-DM patients, the number of CD133(+)PC increased on day 3 following AMI (P = 0.0001). In contrast, no changes were observed in AMI patients with T2DM. Regarding the function of CD133(+)PC, an enhanced chemotactic response was observed following AMI in both non-DM (P = 0.0001) and T2DM (P = 0.007). However, the AMI-related functional activation was significantly weaker in diabetic patients (P = 0.001). Moreover, the expression of catalase was lower in CD133(+)PC from T2DM. Our results show that T2DM not only limits the abundance of CD133(+)PC following AMI, but also limits their activation. This might be explained by a lower resistance of CD133(+)PC to oxidative stress. Our data provide a possible explanation for the delayed postischaemic vascular healing and myocardial recovery in DM.
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