Abstract
The number of circulating stem cells with endothelial progenitor capacity (EPCs) inversely correlates with the number of cardiovascular risk factors. In this study we sought to investigate the effects of vascular H2O2 on circulating EPC levels. In C57BL/6 mice 3 weeks of freely moving or forced physical activity or voluntary exercise failed to increase circulating EPCs defined as double positive for Flk-1 and CD34, CD133 or Sca-1. Likewise, neither insertion of additional genes encoding for catalase (cat++) or eNOS nor eNOS knock-out changed EPCs in resting mice. In striking contrast, inhibition of catalase by aminotriazole strongly reduced circulating EPCs in sedentary cat++ and their transgen-negative littermates (catn), while forced or voluntary exercise training of cat++ mice significantly increased the number of circulating EPCs. The latter effect was completely inhibitable by aminotriazole. These data suggest that endogenous vascular H2O2 likely contributes to the impairment of important stem cell-induced vascular repair mechanisms in cardiovascular disease.
Acknowledgements
This study was supported by the Forschungskommission of the Heinrich-Heine-University Duesseldorf (project 9772272, to G.K. and project 9772 345 to T.S.).
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
This paper was first published online on Early Online on 19 November 2009.