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Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells

Ischemia–reperfusion injury (IRI) in the myocardium has been thoroughly researched, especially in acute coronary syndrome and heart transplantation. However, our understanding of IRI implications on cardiac valves is still developing. This knowledge gap becomes even more pronounced given the advent...

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Autores principales: Kwon, Jennie H., Atteya, Miriam, Mitta, Alekhya, Vogel, Andrew D., Norris, Russell A., Rajab, Taufiek Konrad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607149/
https://www.ncbi.nlm.nih.gov/pubmed/37887883
http://dx.doi.org/10.3390/jcdd10100436
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author Kwon, Jennie H.
Atteya, Miriam
Mitta, Alekhya
Vogel, Andrew D.
Norris, Russell A.
Rajab, Taufiek Konrad
author_facet Kwon, Jennie H.
Atteya, Miriam
Mitta, Alekhya
Vogel, Andrew D.
Norris, Russell A.
Rajab, Taufiek Konrad
author_sort Kwon, Jennie H.
collection PubMed
description Ischemia–reperfusion injury (IRI) in the myocardium has been thoroughly researched, especially in acute coronary syndrome and heart transplantation. However, our understanding of IRI implications on cardiac valves is still developing. This knowledge gap becomes even more pronounced given the advent of partial heart transplantation, a procedure designed to implant isolated human heart valves in young patients. This study aims to investigate the effects of IRI on aortic valvular endothelial cells (VECs), valvular interstitial cells (VICs), and whole leaflet cultures (no separation of VECs and VICs). We employed two conditions: hypoxic cold storage reperfusion (HCSR) and normothermia (NT). Key markers, secreted protein acidic and cysteine rich (SPARC) (osteonectin), and inducible nitric oxide synthase (iNOS2) were evaluated. In the isolated cells under HCSR, VICs manifested a significant 15-fold elevation in SPARC expression compared to NT (p = 0.0016). Conversely, whole leaflet cultures exhibited a 1-fold increment in SPARC expression in NT over HCSR (p = 0.0011). iNOS2 expression in VECs presented a marginal rise in HCSR, whereas, in whole leaflet settings, there was a 1-fold ascent in NT compared to HCSR (p = 0.0003). Minor escalations in the adhesion molecules intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM), E-selection, and P-selection were detected in HCSR for whole leaflet cultures, albeit without statistical significance. Additionally, under HCSR, VICs released a markedly higher quantity of IL-6 and IL-8, with respective p-values of 0.0033 and <0.0001. Interestingly, the IL-6 levels in VECs remained consistent across both HCSR and NT conditions. These insights lay the groundwork for understanding graft IRI following partial heart transplantation and hint at the interdependent dynamic of VECs and VICs in valvular tissue.
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spelling pubmed-106071492023-10-28 Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells Kwon, Jennie H. Atteya, Miriam Mitta, Alekhya Vogel, Andrew D. Norris, Russell A. Rajab, Taufiek Konrad J Cardiovasc Dev Dis Article Ischemia–reperfusion injury (IRI) in the myocardium has been thoroughly researched, especially in acute coronary syndrome and heart transplantation. However, our understanding of IRI implications on cardiac valves is still developing. This knowledge gap becomes even more pronounced given the advent of partial heart transplantation, a procedure designed to implant isolated human heart valves in young patients. This study aims to investigate the effects of IRI on aortic valvular endothelial cells (VECs), valvular interstitial cells (VICs), and whole leaflet cultures (no separation of VECs and VICs). We employed two conditions: hypoxic cold storage reperfusion (HCSR) and normothermia (NT). Key markers, secreted protein acidic and cysteine rich (SPARC) (osteonectin), and inducible nitric oxide synthase (iNOS2) were evaluated. In the isolated cells under HCSR, VICs manifested a significant 15-fold elevation in SPARC expression compared to NT (p = 0.0016). Conversely, whole leaflet cultures exhibited a 1-fold increment in SPARC expression in NT over HCSR (p = 0.0011). iNOS2 expression in VECs presented a marginal rise in HCSR, whereas, in whole leaflet settings, there was a 1-fold ascent in NT compared to HCSR (p = 0.0003). Minor escalations in the adhesion molecules intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM), E-selection, and P-selection were detected in HCSR for whole leaflet cultures, albeit without statistical significance. Additionally, under HCSR, VICs released a markedly higher quantity of IL-6 and IL-8, with respective p-values of 0.0033 and <0.0001. Interestingly, the IL-6 levels in VECs remained consistent across both HCSR and NT conditions. These insights lay the groundwork for understanding graft IRI following partial heart transplantation and hint at the interdependent dynamic of VECs and VICs in valvular tissue. MDPI 2023-10-19 /pmc/articles/PMC10607149/ /pubmed/37887883 http://dx.doi.org/10.3390/jcdd10100436 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kwon, Jennie H.
Atteya, Miriam
Mitta, Alekhya
Vogel, Andrew D.
Norris, Russell A.
Rajab, Taufiek Konrad
Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells
title Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells
title_full Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells
title_fullStr Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells
title_full_unstemmed Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells
title_short Ischemia–Reperfusion Injury in Porcine Aortic Valvular Endothelial and Interstitial Cells
title_sort ischemia–reperfusion injury in porcine aortic valvular endothelial and interstitial cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607149/
https://www.ncbi.nlm.nih.gov/pubmed/37887883
http://dx.doi.org/10.3390/jcdd10100436
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