Endogenous resident c-Kit cardiac stem cells increase in mice with an exercise-induced, physiologically hypertrophied heart

Physical activity evokes well-known adaptations in the cardiovascular system. Although exercise training induces cardiac remodeling, whether multipotent stem cells play a functional role in the hypertrophic process remains unknown. To evaluate this possibility, C57BL/6 mice were subjected to swimmin...

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Main Authors: Camila Ferreira Leite, Carolina Salomão Lopes, Angélica Cristina Alves, Caroline Santos Capitelli Fuzaro, Marcos Vinícius Silva, Lucas Felipe de Oliveira, Lidiane Pereira Garcia, Thaís Soares Farnesi, Marília Beatriz de Cuba, Lenaldo Branco Rocha, Virmondes Rodrigues Jr., Carlo José Freire de Oliveira, Valdo José Dias da Silva
Format: Article
Language:English
Published: Elsevier 2015-07-01
Series:Stem Cell Research
Online Access:http://www.sciencedirect.com/science/article/pii/S1873506115000707
Description
Summary:Physical activity evokes well-known adaptations in the cardiovascular system. Although exercise training induces cardiac remodeling, whether multipotent stem cells play a functional role in the hypertrophic process remains unknown. To evaluate this possibility, C57BL/6 mice were subjected to swimming training aimed at achieving cardiac hypertrophy, which was morphologically and electrocardiographically characterized. Subsequently, c-Kit+Lin− and Sca-1+Lin− cardiac stem cells (CSCs) were quantified using flow cytometry while cardiac muscle-derived stromal cells (CMSCs, also known as cardiac-derived mesenchymal stem cells) were assessed using in vitro colony-forming unit fibroblast assay (CFU-F). Only the number of c-Kit+Lin− cells increased in the hypertrophied heart. To investigate a possible extracardiac origin of these cells, a parabiotic eGFP transgenic/wild-type mouse model was used. The parabiotic pairs were subjected to swimming, and the wild-type heart in particular was tested for eGFP+ stem cells. The results revealed a negligible number of extracardiac stem cells in the heart, allowing us to infer a cardiac origin for the increased amount of detected c-Kit+ cells. In conclusion, the number of resident Sca-1+Lin− cells and CMSCs was not changed, whereas the number of c-Kit+Lin− cells was increased during physiological cardiac hypertrophy. These c-Kit+Lin− CSCs may contribute to the physiological cardiac remodeling that result from exercise training.
ISSN:1873-5061
1876-7753