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Published on: January 25, 2019
Pediatric End-Stage Failing Hearts Demonstrate Increased Cardiac Stem Cells
Brody Wehman1, Sudhish Sharma1, Rachana Mishra1
1Division of Cardiac Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Insights
Children with end-stage heart failure have more cardiac stem cells (CSCs), but these cells show reduced telomere length, indicating diminished function. This suggests potential limitations for CSCs as an autologous cell therapy in pediatric heart failure.
Area of Science:
- Pediatric Cardiology
- Stem Cell Biology
- Regenerative Medicine
Background:
- End-stage heart failure (ESHF) in children presents unique challenges.
- Cardiac stem cells (CSCs) are crucial for myocardial repair.
- Understanding CSCs in pediatric ESHF is vital for therapeutic development.
Purpose of the Study:
- To investigate the presence, characteristics, and function of CSCs in pediatric ESHF.
- To compare CSCs in ESHF myocardium with healthy controls.
- To assess the potential of ESHF-derived CSCs for cell therapy.
Main Methods:
- Tissue samples from pediatric ESHF patients undergoing heart transplantation and age-matched controls were analyzed.
- Quantitative real-time PCR and immunofluorescence were used to determine CSC marker expression (c-kit, islet-1).
- Telomere length was measured to assess CSC growth reserve and functional capacity.
Main Results:
- ESHF myocardium showed a 2.0-2.5 fold increase in c-kit(+) and islet-1(+) CSCs compared to controls.
- CSC expression in ESHF was independent of age.
- CSCs from ESHF patients had significantly shorter telomeres (6.3 ± 0.3 kbp vs. 8.1 ± 0.6 kbp), indicating reduced function.
Conclusions:
- Pediatric ESHF myocardium has an increased, age-independent number of CSCs.
- These CSCs exhibit diminished proliferative potential and functionality.
- ESHF-derived CSCs may have limited utility as autologous cell therapy candidates.
Background:
We sought to determine the location, expression, and characterization of cardiac stem cells (CSCs) in children with end-stage heart failure (ESHF). We hypothesized ESHF myocardium would contain an increased number of CSCs relative to age-matched healthy myocardium, and ESHF-derived CSCs would have diminished functional capacity as evidenced by reduced telomere length.
Methods:
Tissue samples were obtained from the explanted hearts of children undergoing heart transplantation with ESHF, defined as New York Heart Association class III or IV and ejection fraction less than 0.20, and from age-matched congenital heart disease patients with normal myocardium. The expression profile of cardiac-specific stem cell markers was determined using quantitative real time polymerase chain reaction and immunofluorescence. Cardiac stem cell growth reserve was assessed with telomere length.
Results:
There were 15 ESHF and 15 age-matched congenital heart disease patients. End-stage heart failure myocardium demonstrated increased expression of c-kit(+) and islet-1(+) CSCs by 2.0- and 2.5-fold, respectively, compared with myocardium from congenital heart disease patients. There was no difference in expression of c-kit(+) CSCs with advancing age from infants to children in ESHF myocardium. The c-kit(+) CSCs isolated from ESHF patients demonstrated significantly reduced telomere length, suggesting a diminished functional capability in these cells (8.1 ± 0.6 kbp versus 6.3 ± 0.3 kbp; p = 0.015).
Conclusions:
End-stage heart failure myocardium demonstrated an age-independent increase in CSCs relative to healthy myocardium; however, these CSCs from ESHF patients may have diminished proliferative ability and reduced functionality as an autologous cell therapy candidate. Further investigation is necessary to determine the role of ESHF-derived CSCs within the myocardium.
