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TRPA1 as Target in Myocardial Infarction
Transient receptor potential cation channel subfamily A member 1 (TRPA1), an ion channel primarily expressed on sensory neurons, can be activated by substances occurring during myocardial infarction. Aims were to investigate whether activation, inhibition, or absence of TRPA1 affects infarcts and to...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917254/ https://www.ncbi.nlm.nih.gov/pubmed/36768836 http://dx.doi.org/10.3390/ijms24032516 |
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author | Hoebart, Clara Kiss, Attila Pilz, Patrick M. Szabo, Petra L. Podesser, Bruno K. Fischer, Michael J. M. Heber, Stefan |
author_facet | Hoebart, Clara Kiss, Attila Pilz, Patrick M. Szabo, Petra L. Podesser, Bruno K. Fischer, Michael J. M. Heber, Stefan |
author_sort | Hoebart, Clara |
collection | PubMed |
description | Transient receptor potential cation channel subfamily A member 1 (TRPA1), an ion channel primarily expressed on sensory neurons, can be activated by substances occurring during myocardial infarction. Aims were to investigate whether activation, inhibition, or absence of TRPA1 affects infarcts and to explore underlying mechanisms. In the context of myocardial infarction, rats received a TRPA1 agonist, an antagonist, or vehicle at different time points, and infarct size was assessed. Wild type and TRPA1 knockout mice were also compared in this regard. In vitro, sensory neurons were co-cultured with cardiomyocytes and subjected to a model of ischemia-reperfusion. Although there was a difference between TRPA1 activation or inhibition in vivo, no experimental group was different to control animals in infarct size, which also applies to animals lacking TRPA1. In vitro, survival probability of cardiomyocytes challenged by ischemia-reperfusion increased from 32.8% in absence to 45.1% in presence of sensory neurons, which depends, at least partly, on TRPA1. This study raises doubts about whether TRPA1 is a promising target to reduce myocardial damage within a 24 h period. The results are incompatible with relevant enlargements of infarcts by TRPA1 activation or inhibition, which argues against adverse effects when TRPA1 is targeted for other indications. |
format | Online Article Text |
id | pubmed-9917254 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99172542023-02-11 TRPA1 as Target in Myocardial Infarction Hoebart, Clara Kiss, Attila Pilz, Patrick M. Szabo, Petra L. Podesser, Bruno K. Fischer, Michael J. M. Heber, Stefan Int J Mol Sci Article Transient receptor potential cation channel subfamily A member 1 (TRPA1), an ion channel primarily expressed on sensory neurons, can be activated by substances occurring during myocardial infarction. Aims were to investigate whether activation, inhibition, or absence of TRPA1 affects infarcts and to explore underlying mechanisms. In the context of myocardial infarction, rats received a TRPA1 agonist, an antagonist, or vehicle at different time points, and infarct size was assessed. Wild type and TRPA1 knockout mice were also compared in this regard. In vitro, sensory neurons were co-cultured with cardiomyocytes and subjected to a model of ischemia-reperfusion. Although there was a difference between TRPA1 activation or inhibition in vivo, no experimental group was different to control animals in infarct size, which also applies to animals lacking TRPA1. In vitro, survival probability of cardiomyocytes challenged by ischemia-reperfusion increased from 32.8% in absence to 45.1% in presence of sensory neurons, which depends, at least partly, on TRPA1. This study raises doubts about whether TRPA1 is a promising target to reduce myocardial damage within a 24 h period. The results are incompatible with relevant enlargements of infarcts by TRPA1 activation or inhibition, which argues against adverse effects when TRPA1 is targeted for other indications. MDPI 2023-01-28 /pmc/articles/PMC9917254/ /pubmed/36768836 http://dx.doi.org/10.3390/ijms24032516 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 Hoebart, Clara Kiss, Attila Pilz, Patrick M. Szabo, Petra L. Podesser, Bruno K. Fischer, Michael J. M. Heber, Stefan TRPA1 as Target in Myocardial Infarction |
title | TRPA1 as Target in Myocardial Infarction |
title_full | TRPA1 as Target in Myocardial Infarction |
title_fullStr | TRPA1 as Target in Myocardial Infarction |
title_full_unstemmed | TRPA1 as Target in Myocardial Infarction |
title_short | TRPA1 as Target in Myocardial Infarction |
title_sort | trpa1 as target in myocardial infarction |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917254/ https://www.ncbi.nlm.nih.gov/pubmed/36768836 http://dx.doi.org/10.3390/ijms24032516 |
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