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    <p>We aimed to identify and quantify CD117<sup>+</sup> and CD90<sup>+</sup> endogenous cardiac progenitor cells (CPC) in human healthy and diseased hearts. We hypothesize that these cells perform a locally acting, contributing function in overcoming medical conditions of the heart by endogenous means. Human myocardium biopsies were obtained from 23 patients with the following diagnoses: Dilatative cardiomyopathy (DCM), ischemic cardiomyopathy (ICM), myocarditis, and controls from healthy cardiac patients. High-resolution scanning microscopy of the whole slide enabled a computer-based immunohistochemical quantification of CD117 and CD90. Those signals were evaluated by Definiens Tissue Phenomics® Technology. Co-localization of CD117 and CD90 was determined by analyzing comparable serial sections. CD117<sup>+</sup>/CD90<sup>+</sup> cardiac cells were detected in all biopsies. The highest expression of CD90 was revealed in the myocarditis group. CD117 was significantly higher in all patient groups, compared to healthy specimens (<sup>*</sup>p < 0.05). The highest co-expression was found in the myocarditis group (6.75 ± 3.25 CD90<sup>+</sup>CD117<sup>+</sup> cells/mm<sup>2</sup>) followed by ICM (4 ± 1.89 cells/mm<sup>2</sup>), DCM (1.67 ± 0.58 cells/mm<sup>2</sup>), and healthy specimens (1 ± 0.43 cells/mm<sup>2</sup>). We conclude that the human heart comprises a fraction of local CD117<sup>+</sup> and CD90<sup>+</sup> cells. We hypothesize that these cells are part of local endogenous progenitor cells due to the co-expression of CD90 and CD117. With novel digital image analysis technologies, a quantification of the CD117 and CD90 signals is available. Our experiments reveal an increase of CD117 and CD90 in patients with myocarditis.</p
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