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Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload

Sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) and sarcolemmal Na(+)/Ca(2+) exchanger (NCX1) structures are involved in heart cell Ca(2+) homeostasis. Previous studies have shown discrepancies in their function and expression in heart failure. The goal of this study was to evaluate heart function an...

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Autores principales: Mazeto, I.F.S., Okoshi, K., Silveira, C.F.S.M.P., Sant'Ana, P.G., da Silva, V.L., Mota, G.A.F., de Souza, S.L.B., Vileigas, D.F., Padovani, C.R., Cicogna, A.C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Associação Brasileira de Divulgação Científica 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7894392/
https://www.ncbi.nlm.nih.gov/pubmed/33624728
http://dx.doi.org/10.1590/1414-431X202010138
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author Mazeto, I.F.S.
Okoshi, K.
Silveira, C.F.S.M.P.
Sant'Ana, P.G.
da Silva, V.L.
Mota, G.A.F.
de Souza, S.L.B.
Vileigas, D.F.
Padovani, C.R.
Cicogna, A.C.
author_facet Mazeto, I.F.S.
Okoshi, K.
Silveira, C.F.S.M.P.
Sant'Ana, P.G.
da Silva, V.L.
Mota, G.A.F.
de Souza, S.L.B.
Vileigas, D.F.
Padovani, C.R.
Cicogna, A.C.
author_sort Mazeto, I.F.S.
collection PubMed
description Sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) and sarcolemmal Na(+)/Ca(2+) exchanger (NCX1) structures are involved in heart cell Ca(2+) homeostasis. Previous studies have shown discrepancies in their function and expression in heart failure. The goal of this study was to evaluate heart function and hypertrophied muscle Ca(2+)-handling protein behavior under pressure overload. Twenty male Wistar rats were divided into two groups: Aortic stenosis (AoS), induced by a clip placed at the beginning of the aorta, and Control (Sham). After 18 weeks, heart function and structure were evaluated by echocardiogram. Myocardial function was analyzed by isolated papillary muscle (IPM) at basal condition and Ca(2+) protein functions were evaluated after post-pause contraction and blockage with cyclopiazonic acid in IPM. Ca(2+)-handling protein expression was studied by western blot (WB). Echocardiogram showed that AoS caused concentric hypertrophy with enhanced ejection fraction and diastolic dysfunction inferred by dilated left atrium and increased relative wall thickness. IPM study showed developed tension was the same in both groups. AoS showed increased stiffness revealed by enhanced resting tension, and changes in Ca(2+) homeostasis shown by calcium elevation and SERCA2a blockage maneuvers. WB revealed decreased NCX1, SERCA2a, and phosphorylated phospholambam (PLB) on serine-16 in AoS. AoS had left ventricular hypertrophy and diastolic dysfunction compared to Sham; this could be related to our findings regarding calcium homeostasis behavior: deficit in NCX1, SERCA2a, and phosphorylated PLB on serine-16.
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spelling pubmed-78943922021-02-26 Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload Mazeto, I.F.S. Okoshi, K. Silveira, C.F.S.M.P. Sant'Ana, P.G. da Silva, V.L. Mota, G.A.F. de Souza, S.L.B. Vileigas, D.F. Padovani, C.R. Cicogna, A.C. Braz J Med Biol Res Research Article Sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) and sarcolemmal Na(+)/Ca(2+) exchanger (NCX1) structures are involved in heart cell Ca(2+) homeostasis. Previous studies have shown discrepancies in their function and expression in heart failure. The goal of this study was to evaluate heart function and hypertrophied muscle Ca(2+)-handling protein behavior under pressure overload. Twenty male Wistar rats were divided into two groups: Aortic stenosis (AoS), induced by a clip placed at the beginning of the aorta, and Control (Sham). After 18 weeks, heart function and structure were evaluated by echocardiogram. Myocardial function was analyzed by isolated papillary muscle (IPM) at basal condition and Ca(2+) protein functions were evaluated after post-pause contraction and blockage with cyclopiazonic acid in IPM. Ca(2+)-handling protein expression was studied by western blot (WB). Echocardiogram showed that AoS caused concentric hypertrophy with enhanced ejection fraction and diastolic dysfunction inferred by dilated left atrium and increased relative wall thickness. IPM study showed developed tension was the same in both groups. AoS showed increased stiffness revealed by enhanced resting tension, and changes in Ca(2+) homeostasis shown by calcium elevation and SERCA2a blockage maneuvers. WB revealed decreased NCX1, SERCA2a, and phosphorylated phospholambam (PLB) on serine-16 in AoS. AoS had left ventricular hypertrophy and diastolic dysfunction compared to Sham; this could be related to our findings regarding calcium homeostasis behavior: deficit in NCX1, SERCA2a, and phosphorylated PLB on serine-16. Associação Brasileira de Divulgação Científica 2021-02-12 /pmc/articles/PMC7894392/ /pubmed/33624728 http://dx.doi.org/10.1590/1414-431X202010138 Text en https://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Mazeto, I.F.S.
Okoshi, K.
Silveira, C.F.S.M.P.
Sant'Ana, P.G.
da Silva, V.L.
Mota, G.A.F.
de Souza, S.L.B.
Vileigas, D.F.
Padovani, C.R.
Cicogna, A.C.
Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
title Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
title_full Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
title_fullStr Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
title_full_unstemmed Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
title_short Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
title_sort calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7894392/
https://www.ncbi.nlm.nih.gov/pubmed/33624728
http://dx.doi.org/10.1590/1414-431X202010138
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