Cargando…
Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion
Lysyl oxidase (LOX) is an enzyme critically involved in collagen maturation, whose activity releases H(2)O(2) as a by-product. Previous studies demonstrated that LOX over-expression enhances reactive oxygen species (ROS) production and exacerbates cardiac remodeling induced by pressure overload. How...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8773108/ https://www.ncbi.nlm.nih.gov/pubmed/35052579 http://dx.doi.org/10.3390/antiox11010075 |
_version_ | 1784636001675640832 |
---|---|
author | Valls-Lacalle, Laura Puertas-Umbert, Lídia Varona, Saray Martínez-González, José Rodríguez, Cristina Rodríguez-Sinovas, Antonio |
author_facet | Valls-Lacalle, Laura Puertas-Umbert, Lídia Varona, Saray Martínez-González, José Rodríguez, Cristina Rodríguez-Sinovas, Antonio |
author_sort | Valls-Lacalle, Laura |
collection | PubMed |
description | Lysyl oxidase (LOX) is an enzyme critically involved in collagen maturation, whose activity releases H(2)O(2) as a by-product. Previous studies demonstrated that LOX over-expression enhances reactive oxygen species (ROS) production and exacerbates cardiac remodeling induced by pressure overload. However, whether LOX influences acute myocardial infarction and post-infarct left ventricular remodeling and the contribution of LOX to myocardial oxidative stress following ischemia-reperfusion have not been analyzed. Isolated hearts from transgenic mice over-expressing human LOX in the heart (TgLOX) and wild-type (WT) littermates were subjected to global ischemia and reperfusion. Although under basal conditions LOX transgenesis is associated with higher cardiac superoxide levels than WT mice, no differences in ROS production were detected in ischemic hearts and a comparable acute ischemia-reperfusion injury was observed (infarct size: 56.24 ± 9.44 vs. 48.63 ± 2.99% of cardiac weight in WT and TgLOX, respectively). Further, similar changes in cardiac dimensions and function were observed in TgLOX and WT mice 28 days after myocardial infarction induced by transient left anterior descending (LAD) coronary artery occlusion, and no differences in scar area were detected (20.29 ± 3.10 vs. 21.83 ± 2.83% of left ventricle). Our data evidence that, although LOX transgenesis induces baseline myocardial oxidative stress, neither ROS production, infarct size, nor post-infarction cardiac remodeling were exacerbated following myocardial ischemia-reperfusion. |
format | Online Article Text |
id | pubmed-8773108 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-87731082022-01-21 Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion Valls-Lacalle, Laura Puertas-Umbert, Lídia Varona, Saray Martínez-González, José Rodríguez, Cristina Rodríguez-Sinovas, Antonio Antioxidants (Basel) Article Lysyl oxidase (LOX) is an enzyme critically involved in collagen maturation, whose activity releases H(2)O(2) as a by-product. Previous studies demonstrated that LOX over-expression enhances reactive oxygen species (ROS) production and exacerbates cardiac remodeling induced by pressure overload. However, whether LOX influences acute myocardial infarction and post-infarct left ventricular remodeling and the contribution of LOX to myocardial oxidative stress following ischemia-reperfusion have not been analyzed. Isolated hearts from transgenic mice over-expressing human LOX in the heart (TgLOX) and wild-type (WT) littermates were subjected to global ischemia and reperfusion. Although under basal conditions LOX transgenesis is associated with higher cardiac superoxide levels than WT mice, no differences in ROS production were detected in ischemic hearts and a comparable acute ischemia-reperfusion injury was observed (infarct size: 56.24 ± 9.44 vs. 48.63 ± 2.99% of cardiac weight in WT and TgLOX, respectively). Further, similar changes in cardiac dimensions and function were observed in TgLOX and WT mice 28 days after myocardial infarction induced by transient left anterior descending (LAD) coronary artery occlusion, and no differences in scar area were detected (20.29 ± 3.10 vs. 21.83 ± 2.83% of left ventricle). Our data evidence that, although LOX transgenesis induces baseline myocardial oxidative stress, neither ROS production, infarct size, nor post-infarction cardiac remodeling were exacerbated following myocardial ischemia-reperfusion. MDPI 2021-12-29 /pmc/articles/PMC8773108/ /pubmed/35052579 http://dx.doi.org/10.3390/antiox11010075 Text en © 2021 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 Valls-Lacalle, Laura Puertas-Umbert, Lídia Varona, Saray Martínez-González, José Rodríguez, Cristina Rodríguez-Sinovas, Antonio Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion |
title | Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion |
title_full | Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion |
title_fullStr | Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion |
title_full_unstemmed | Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion |
title_short | Human Lysyl Oxidase Over-Expression Enhances Baseline Cardiac Oxidative Stress but Does Not Aggravate ROS Generation or Infarct Size Following Myocardial Ischemia-Reperfusion |
title_sort | human lysyl oxidase over-expression enhances baseline cardiac oxidative stress but does not aggravate ros generation or infarct size following myocardial ischemia-reperfusion |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8773108/ https://www.ncbi.nlm.nih.gov/pubmed/35052579 http://dx.doi.org/10.3390/antiox11010075 |
work_keys_str_mv | AT vallslacallelaura humanlysyloxidaseoverexpressionenhancesbaselinecardiacoxidativestressbutdoesnotaggravaterosgenerationorinfarctsizefollowingmyocardialischemiareperfusion AT puertasumbertlidia humanlysyloxidaseoverexpressionenhancesbaselinecardiacoxidativestressbutdoesnotaggravaterosgenerationorinfarctsizefollowingmyocardialischemiareperfusion AT varonasaray humanlysyloxidaseoverexpressionenhancesbaselinecardiacoxidativestressbutdoesnotaggravaterosgenerationorinfarctsizefollowingmyocardialischemiareperfusion AT martinezgonzalezjose humanlysyloxidaseoverexpressionenhancesbaselinecardiacoxidativestressbutdoesnotaggravaterosgenerationorinfarctsizefollowingmyocardialischemiareperfusion AT rodriguezcristina humanlysyloxidaseoverexpressionenhancesbaselinecardiacoxidativestressbutdoesnotaggravaterosgenerationorinfarctsizefollowingmyocardialischemiareperfusion AT rodriguezsinovasantonio humanlysyloxidaseoverexpressionenhancesbaselinecardiacoxidativestressbutdoesnotaggravaterosgenerationorinfarctsizefollowingmyocardialischemiareperfusion |