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Recent studies have found that cardiac stem cells (CSCs) are present in the adult heart. CSCs play an important role in maintaining the balance of the number of myocardial cells. The purpose of this study was to examine characteristics of human CSCs and their correlation with clinical characteristics of patients. We collected heart auricles of 105 patients (age range, 1-78 years; mean, 55.6 ± 17.0 years) undergoing cardiac surgery to obtain CSCs. We assayed the percentage of c-kit positive (c-kit(+)) CSCs with flow cytometry. Plasma N(ɛ)-(carboxymethyl)lysine (CML) concentrations were measured by enzyme-linked immunosorbent assay. The percentage of c-kit(+) CSCs was 4.96 ± 3.12% (0.98-17.17%), and this was significantly negatively correlated with age, the presence of diabetes mellitus (DM) and coronary heart disease (CHD) (r values were -0.797 [P < 0.01], -0.500 [P < 0.01] and -0.250 [P = 0.011], respectively). The percentage of c-kit(+) CSCs was significantly negatively correlated with CML concentrations (r = -0.859, P < 0.01). The percentage of c-kit(+) CSCs decreases with ageing and is further decreased in patients with DM and/or CHD. Furthermore, plasma CML concentrations may have potential as an indicator of the number of c-kit(+) CSCs., (© The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Background:  Stem cells transplanted to the ischemic myocardium usually encounter massive cell death within a few days after transplantation, and hypoxic preconditioning (HPC) is currently used as a strategy to prepare stem cells for increased survival and engraftment in the heart. The purpose of this study is to determine whether Pim-1 kinase mediates any beneficial effects of HPC for human cardiac progenitor cells (CPCs)., Methods and Results:  Human CPCs were isolated from an adult heart auricle and were purified by magnetic-activated cell sorting using c-kit magnetic beads; they were hypoxic preconditioned for 6h. Both Pim-1 and p-Akt were determined. CPCs were assigned to one of the following groups: (1) control (without HPC); (2) HPC; or (3) HPC+I (Pim-1 inhibitor). HPC can promote the survival of CPCs. HPC enhances the expression of Pim-1 kinase in a time-dependent manner, which causes a reduction of proapoptotic elements (cytochrome c and cleaved caspase-3) and the preservation/modulation of important components of the mitochondria (Bcl-2, Bcl-XL and p-Bad), and attenuates mitochondrial damages. All of these protective effects were blocked by a Pim-1 inhibitor., Conclusions:  Pim-1 plays a pivotal role in the protective effect of HPC for CPCs, and the promotion of the expression of Pim-1 in CPCs can as serve part of molecular therapeutic interventional strategies in the treatment of cardiomyopathy damage by blunting CPC death.