Brain-dead donor heart conservation with a preservation solution supplemented by a conditioned medium from mesenchymal stem cells improves graft contractility after transplantation

• Verfasst von: Korkmaz-İçöz, Sevil [VerfasserIn]
• Verfasst von: Li, Kunsheng [VerfasserIn]
• Verfasst von: Loganathan, Sivakkanan [VerfasserIn]
• Verfasst von: Ding, Qingwei [VerfasserIn]
• Verfasst von: Ruppert, Mihály [VerfasserIn]
• Verfasst von: Radovits, Tamás [VerfasserIn]
• Verfasst von: Brlecic, Paige [VerfasserIn]
• Verfasst von: Sayour, Alex A [VerfasserIn]
• Verfasst von: Karck, Matthias [VerfasserIn]
• Verfasst von: Szabó, Gábor [VerfasserIn]
• Titel: Brain-dead donor heart conservation with a preservation solution supplemented by a conditioned medium from mesenchymal stem cells improves graft contractility after transplantation
• Verf.angabe: Sevil Korkmaz-Icöz, Kunsheng Li, Sivakkanan Loganathan, Qingwei Ding, Mihály Ruppert, Tamás Radovits, Paige Brlecic, Alex A Sayour, Matthias Karck, Gábor Szabó
• Jahr: 2020
• Umfang: 10 S.
• Illustrationen: Diagramme
• Fussnoten: First published: 11 March 2020 ; Gesehen am 10.01.2022
• Titel Quelle: Enthalten in: American journal of transplantation
• Ort Quelle: [Amsterdam] : Elsevier, 2001
• Jahr Quelle: 2020
• Band/Heft Quelle: 20(2020), 10, Seite 2847-2856
• ISSN Quelle: 1600-6143
• DOI: doi:10.1111/ajt.15843
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1752228804
• K10plus-PPN:
  Universitätsbibliothek
• Lokale URL UB: Zum Volltext

Abstract

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.