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Diabetes mellitus impairs CD133 + progenitor cell function after myocardial infarction
Author(s) -
Vöö S.,
Dunaeva M.,
Eggermann J.,
Stadler N.,
Waltenberger J.
Publication year - 2009
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2008.02011.x
Subject(s) - medicine , myocardial infarction , progenitor cell , diabetes mellitus , cardiology , coronary artery disease , type 2 diabetes mellitus , endothelial progenitor cell , stem cell , endocrinology , biology , genetics
. Background. 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. Methods. 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. Results. 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. Conclusions. 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.