• Media type: E-Article
  • Title: Brain-dead donor heart conservation with a preservation solution supplemented by a conditioned medium from mesenchymal stem cells improves graft contractility after transplantation
  • Contributor: Korkmaz-İçöz, Sevil [VerfasserIn]; Li, Kunsheng [VerfasserIn]; Loganathan, Sivakkanan [VerfasserIn]; Ding, Qingwei [VerfasserIn]; Ruppert, Mihály [VerfasserIn]; Radovits, Tamás [VerfasserIn]; Brlecic, Paige [VerfasserIn]; Sayour, Alex A [VerfasserIn]; Karck, Matthias [VerfasserIn]; Szabó, Gábor [VerfasserIn]
  • imprint: 2020
  • Published in: American journal of transplantation ; 20(2020), 10, Seite 2847-2856
  • Language: English
  • DOI: 10.1111/ajt.15843
  • ISSN: 1600-6143
  • Identifier:
  • Origination:
  • Footnote: First published: 11 March 2020
  • Description: Hearts are usually procured from brain-dead (BD) donors. However, brain death may induce hemodynamic instability, which may contribute to posttransplant graft dysfunction. We hypothesized that BD-donor heart preservation with a conditioned medium (CM) from mesenchymal stem cells (MSCs) would improve graft function after transplantation. Additionally, we explored the PI3K pathway's potential role. Rat MSCs-derived CM was used for conservation purposes. Donor rats were either exposed to sham operation or brain death by inflation of a subdural balloon-catheter for 5.5 hours. Then, the hearts were explanted, stored in cardioplegic solution-supplemented with either a medium vehicle (BD and sham), CM (BD + CM), or LY294002, an inhibitor of PI3K (BD + CM + LY), and finally transplanted. Systolic performance and relaxation parameters were significantly reduced in BD-donors compared to sham. After transplantation, systolic and diastolic functions were significantly decreased, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells and endonuclease G positive cells were increased in the BD-group compared to sham. Preservation of BD-donor hearts with CM resulted in a recovery of systolic graft function (dP/dtmax: BD + CM: 3148 ± 178 vs BD: 2192 ± 94 mm Hg/s at 110 µL, P < .05) and reduced apoptosis. LY294002 partially lowered graft protection afforded by CM in the BD group. Our data suggest that PI3K/Akt pathway is not the primary mechanism of action of CM in improving posttransplant cardiac contractility and preventing caspase-independent apoptosis.
  • Access State: Open Access
  • Rights information: Attribution - Non Commercial (CC BY-NC)