Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development

The stretch of cardiac muscle increases developed force in two phases. The first phase occurs immediately after stretch and is the expression of the Frank-Starling mechanism, while the second one or slow force response (SFR) occurs gradually and is due to an increase in the calcium transient amplitu...

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Autores principales: Zavala, Maite Raquel, Díaz, Romina Gisel, Villa Abrille, María Celeste, Pérez, Néstor Gustavo
Formato: Articulo
Lenguaje:Inglés
Publicado: 2021
Materias:
SFR
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/124820
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id I19-R120-10915-124820
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Medicina
TRX1
SFR
NHE1
antioxidant
cardiac hypertrophy
spellingShingle Medicina
TRX1
SFR
NHE1
antioxidant
cardiac hypertrophy
Zavala, Maite Raquel
Díaz, Romina Gisel
Villa Abrille, María Celeste
Pérez, Néstor Gustavo
Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development
topic_facet Medicina
TRX1
SFR
NHE1
antioxidant
cardiac hypertrophy
description The stretch of cardiac muscle increases developed force in two phases. The first phase occurs immediately after stretch and is the expression of the Frank-Starling mechanism, while the second one or slow force response (SFR) occurs gradually and is due to an increase in the calcium transient amplitude. An important step in the chain of events leading to the SFR generation is the increased production of reactive oxygen species (ROS) leading to redox sensitive ERK1/2, p90RSK, and NHE1 phosphorylation/activation. Conversely, suppression of ROS production blunts the SFR. The purpose of this study was to explore whether overexpression of the ubiquitously expressed antioxidant molecule thioredoxin-1 (TRX1) affects the SFR development and NHE1 phosphorylation. We did not detect any change in basal phopho-ERK1/2, phopho-p90RSK, and NHE1 expression in mice with TRX1 overexpression compared to wild type (WT). Isolated papillary muscles from WT or TRX1-overexpressing mice were stretched from 92 to 98% of its maximal length. A prominent SFR was observed in WT mice that was completely canceled in TRX1 animals. Interestingly, myocardial stretch induced a significant increase in NHE1 phosphorylation in WT mice that was not detected in TRX1-overexpressing mice. These novel results suggest that magnification of cardiac antioxidant defense power by overexpression of TRX1 precludes NHE1 phosphorylation/activation after stretch, consequently blunting the SFR development.
format Articulo
Articulo
author Zavala, Maite Raquel
Díaz, Romina Gisel
Villa Abrille, María Celeste
Pérez, Néstor Gustavo
author_facet Zavala, Maite Raquel
Díaz, Romina Gisel
Villa Abrille, María Celeste
Pérez, Néstor Gustavo
author_sort Zavala, Maite Raquel
title Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development
title_short Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development
title_full Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development
title_fullStr Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development
title_full_unstemmed Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development
title_sort thioredoxin 1 (trx1) overexpression cancels the slow force response (sfr) development
publishDate 2021
url http://sedici.unlp.edu.ar/handle/10915/124820
work_keys_str_mv AT zavalamaiteraquel thioredoxin1trx1overexpressioncancelstheslowforceresponsesfrdevelopment
AT diazrominagisel thioredoxin1trx1overexpressioncancelstheslowforceresponsesfrdevelopment
AT villaabrillemariaceleste thioredoxin1trx1overexpressioncancelstheslowforceresponsesfrdevelopment
AT pereznestorgustavo thioredoxin1trx1overexpressioncancelstheslowforceresponsesfrdevelopment
bdutipo_str Repositorios
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