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Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis

Introduction: Myocardial remodeling due to large atrial septum defect (ASD) is macroscopically characterized by dilation of the right-sided cardiac cavities secondary to volume overload, the cellular mechanisms of which are not yet understood. We postulated that inflammation, fibrosis, and cell deat...

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Autores principales: Rouatbi, Hatem, Farhat, Nesrine, Heying, Ruth, Gérard, Arlette, Vazquez-Jimenez, Jaime F., Seghaye, Marie-Christine
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033500/
https://www.ncbi.nlm.nih.gov/pubmed/32117843
http://dx.doi.org/10.3389/fped.2020.00040
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author Rouatbi, Hatem
Farhat, Nesrine
Heying, Ruth
Gérard, Arlette
Vazquez-Jimenez, Jaime F.
Seghaye, Marie-Christine
author_facet Rouatbi, Hatem
Farhat, Nesrine
Heying, Ruth
Gérard, Arlette
Vazquez-Jimenez, Jaime F.
Seghaye, Marie-Christine
author_sort Rouatbi, Hatem
collection PubMed
description Introduction: Myocardial remodeling due to large atrial septum defect (ASD) is macroscopically characterized by dilation of the right-sided cardiac cavities secondary to volume overload, the cellular mechanisms of which are not yet understood. We postulated that inflammation, fibrosis, and cell death are actors of right atrial remodeling secondary to ASD. Patients and Methods: In 12 children with large ASD (median age: 63 months), expression of genes coding for proteins involved in the response to cell stress and -protection, inflammation, growth and angiogenesis, fibrosis, and apoptosis was assessed by RT-PCR in right atrial myocardial biopsies taken during cardiac surgery. The presence of cytokines in myocardial cells was confirmed by immunohistochemistry and effective apoptosis by TUNEL assay. Results: In all patients investigated, a cellular response to early mechanical stress with the initiation of early protective mechanisms, of inflammation (and its control), -growth, and -angiogenesis, of fibrosis and apoptosis was present. The apoptotic index assessed by TUNEL assay averaged 0.3%. Conclusions: In children with large ASD, macroscopic right atrial remodeling relates to cellular mechanisms involving the expression of numerous genes that either still act to protect cells and tissues but that also harm as they initiate and/or sustain inflammation, fibrosis, and cell death by apoptosis. This may contribute to long term morbidity in patients with ASD.
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spelling pubmed-70335002020-02-28 Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis Rouatbi, Hatem Farhat, Nesrine Heying, Ruth Gérard, Arlette Vazquez-Jimenez, Jaime F. Seghaye, Marie-Christine Front Pediatr Pediatrics Introduction: Myocardial remodeling due to large atrial septum defect (ASD) is macroscopically characterized by dilation of the right-sided cardiac cavities secondary to volume overload, the cellular mechanisms of which are not yet understood. We postulated that inflammation, fibrosis, and cell death are actors of right atrial remodeling secondary to ASD. Patients and Methods: In 12 children with large ASD (median age: 63 months), expression of genes coding for proteins involved in the response to cell stress and -protection, inflammation, growth and angiogenesis, fibrosis, and apoptosis was assessed by RT-PCR in right atrial myocardial biopsies taken during cardiac surgery. The presence of cytokines in myocardial cells was confirmed by immunohistochemistry and effective apoptosis by TUNEL assay. Results: In all patients investigated, a cellular response to early mechanical stress with the initiation of early protective mechanisms, of inflammation (and its control), -growth, and -angiogenesis, of fibrosis and apoptosis was present. The apoptotic index assessed by TUNEL assay averaged 0.3%. Conclusions: In children with large ASD, macroscopic right atrial remodeling relates to cellular mechanisms involving the expression of numerous genes that either still act to protect cells and tissues but that also harm as they initiate and/or sustain inflammation, fibrosis, and cell death by apoptosis. This may contribute to long term morbidity in patients with ASD. Frontiers Media S.A. 2020-02-14 /pmc/articles/PMC7033500/ /pubmed/32117843 http://dx.doi.org/10.3389/fped.2020.00040 Text en Copyright © 2020 Rouatbi, Farhat, Heying, Gérard, Vazquez-Jimenez and Seghaye. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pediatrics
Rouatbi, Hatem
Farhat, Nesrine
Heying, Ruth
Gérard, Arlette
Vazquez-Jimenez, Jaime F.
Seghaye, Marie-Christine
Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis
title Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis
title_full Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis
title_fullStr Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis
title_full_unstemmed Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis
title_short Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis
title_sort right atrial myocardial remodeling in children with atrial septal defect involves inflammation, growth, fibrosis, and apoptosis
topic Pediatrics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033500/
https://www.ncbi.nlm.nih.gov/pubmed/32117843
http://dx.doi.org/10.3389/fped.2020.00040
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