Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1159/000481876 http://hdl.handle.net/11449/175341 |
Resumo: | Background/Aims: This study aimed to discern whether the cardiac alterations caused by retinoic acid (RA) in normal adult rats are physiologic or pathologic. Methods and Results: Wistar rats were assigned into four groups: control animals (C, n = 20) received a standard rat chow; animals fed a diet supplemented with 0.3 mg/kg/day all-trans-RA (AR1, n = 20); animals fed a diet supplemented with 5 mg/kg/day all-trans-RA (AR2, n = 20); and animals fed a diet supplemented with 10 mg/kg/day all-trans-RA (AR3, n = 20). After 2 months, the animals were submitted to echocardiogram, isolated heart study, histology, energy metabolism status, oxidative stress condition, and the signaling pathway involved in the cardiac remodeling induced by RA. RA increased myocyte cross-sectional area in a dose-dependent manner. The treatment did not change the morphological and functional variables, assessed by echocardiogram and isolated heart study. In contrast, RA changed catalases, superoxide dismutase, and glutathione peroxidases and was associated with increased values of lipid hydroperoxide, suggesting oxidative stress. RA also reduced citrate synthase, enzymatic mitochondrial complex II, ATP synthase, and enzymes of fatty acid metabolism and was associated with increased enzymes involved in glucose use. In addition, RA increased JNK 1/2 expression, without changes in TGF-β, PI3K, AKT, NFκB, S6K, and ERK. Conclusion: In normal rats, RA induces cardiac hypertrophy in a dose-dependent manner. The non-participation of the PI3K/Akt pathway, associated with the participation of the JNK pathway, oxidative stress, and changes in energy metabolism, suggests that cardiac remodeling induced by RA supplementation is deleterious. |
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Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal RatsCardiac functionEnergy metabolismHypertrophyRetinoic acidBackground/Aims: This study aimed to discern whether the cardiac alterations caused by retinoic acid (RA) in normal adult rats are physiologic or pathologic. Methods and Results: Wistar rats were assigned into four groups: control animals (C, n = 20) received a standard rat chow; animals fed a diet supplemented with 0.3 mg/kg/day all-trans-RA (AR1, n = 20); animals fed a diet supplemented with 5 mg/kg/day all-trans-RA (AR2, n = 20); and animals fed a diet supplemented with 10 mg/kg/day all-trans-RA (AR3, n = 20). After 2 months, the animals were submitted to echocardiogram, isolated heart study, histology, energy metabolism status, oxidative stress condition, and the signaling pathway involved in the cardiac remodeling induced by RA. RA increased myocyte cross-sectional area in a dose-dependent manner. The treatment did not change the morphological and functional variables, assessed by echocardiogram and isolated heart study. In contrast, RA changed catalases, superoxide dismutase, and glutathione peroxidases and was associated with increased values of lipid hydroperoxide, suggesting oxidative stress. RA also reduced citrate synthase, enzymatic mitochondrial complex II, ATP synthase, and enzymes of fatty acid metabolism and was associated with increased enzymes involved in glucose use. In addition, RA increased JNK 1/2 expression, without changes in TGF-β, PI3K, AKT, NFκB, S6K, and ERK. Conclusion: In normal rats, RA induces cardiac hypertrophy in a dose-dependent manner. The non-participation of the PI3K/Akt pathway, associated with the participation of the JNK pathway, oxidative stress, and changes in energy metabolism, suggests that cardiac remodeling induced by RA supplementation is deleterious.São Paulo State University (Unesp) Botucatu Medical School Internal Medicine DepartmentSão Paulo State University (Unesp) Institute of Biosciences of Botucatu Chemistry and Biochemistry DepartmentSão Paulo State University (Unesp) Botucatu Medical School Internal Medicine DepartmentSão Paulo State University (Unesp) Institute of Biosciences of Botucatu Chemistry and Biochemistry DepartmentUniversidade Estadual Paulista (Unesp)Silva, Renata A. C. [UNESP]Gonçalves, Andréa F. [UNESP]Dos Santos, Priscila P. [UNESP]Rafacho, Bruna [UNESP]Claro, Renan F. T. [UNESP]Minicucci, Marcos F. [UNESP]Azevedo, Paula S. [UNESP]Polegato, Bertha F. [UNESP]Zanati, Silméia G. [UNESP]Fernandes, Ana Angélica [UNESP]Paiva, Sergio A. R. [UNESP]Zornoff, Leonardo A. M. [UNESP]2018-12-11T17:15:24Z2018-12-11T17:15:24Z2017-11-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1449-1459application/pdfhttp://dx.doi.org/10.1159/000481876Cellular Physiology and Biochemistry, v. 43, n. 4, p. 1449-1459, 2017.1421-97781015-8987http://hdl.handle.net/11449/17534110.1159/0004818762-s2.0-850314095862-s2.0-85031409586.pdfScopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengCellular Physiology and Biochemistry1,5611,561info:eu-repo/semantics/openAccess2024-01-18T06:33:26Zoai:repositorio.unesp.br:11449/175341Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-01-18T06:33:26Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
title |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
spellingShingle |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats Silva, Renata A. C. [UNESP] Cardiac function Energy metabolism Hypertrophy Retinoic acid |
title_short |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
title_full |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
title_fullStr |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
title_full_unstemmed |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
title_sort |
Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats |
author |
Silva, Renata A. C. [UNESP] |
author_facet |
Silva, Renata A. C. [UNESP] Gonçalves, Andréa F. [UNESP] Dos Santos, Priscila P. [UNESP] Rafacho, Bruna [UNESP] Claro, Renan F. T. [UNESP] Minicucci, Marcos F. [UNESP] Azevedo, Paula S. [UNESP] Polegato, Bertha F. [UNESP] Zanati, Silméia G. [UNESP] Fernandes, Ana Angélica [UNESP] Paiva, Sergio A. R. [UNESP] Zornoff, Leonardo A. M. [UNESP] |
author_role |
author |
author2 |
Gonçalves, Andréa F. [UNESP] Dos Santos, Priscila P. [UNESP] Rafacho, Bruna [UNESP] Claro, Renan F. T. [UNESP] Minicucci, Marcos F. [UNESP] Azevedo, Paula S. [UNESP] Polegato, Bertha F. [UNESP] Zanati, Silméia G. [UNESP] Fernandes, Ana Angélica [UNESP] Paiva, Sergio A. R. [UNESP] Zornoff, Leonardo A. M. [UNESP] |
author2_role |
author author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Silva, Renata A. C. [UNESP] Gonçalves, Andréa F. [UNESP] Dos Santos, Priscila P. [UNESP] Rafacho, Bruna [UNESP] Claro, Renan F. T. [UNESP] Minicucci, Marcos F. [UNESP] Azevedo, Paula S. [UNESP] Polegato, Bertha F. [UNESP] Zanati, Silméia G. [UNESP] Fernandes, Ana Angélica [UNESP] Paiva, Sergio A. R. [UNESP] Zornoff, Leonardo A. M. [UNESP] |
dc.subject.por.fl_str_mv |
Cardiac function Energy metabolism Hypertrophy Retinoic acid |
topic |
Cardiac function Energy metabolism Hypertrophy Retinoic acid |
description |
Background/Aims: This study aimed to discern whether the cardiac alterations caused by retinoic acid (RA) in normal adult rats are physiologic or pathologic. Methods and Results: Wistar rats were assigned into four groups: control animals (C, n = 20) received a standard rat chow; animals fed a diet supplemented with 0.3 mg/kg/day all-trans-RA (AR1, n = 20); animals fed a diet supplemented with 5 mg/kg/day all-trans-RA (AR2, n = 20); and animals fed a diet supplemented with 10 mg/kg/day all-trans-RA (AR3, n = 20). After 2 months, the animals were submitted to echocardiogram, isolated heart study, histology, energy metabolism status, oxidative stress condition, and the signaling pathway involved in the cardiac remodeling induced by RA. RA increased myocyte cross-sectional area in a dose-dependent manner. The treatment did not change the morphological and functional variables, assessed by echocardiogram and isolated heart study. In contrast, RA changed catalases, superoxide dismutase, and glutathione peroxidases and was associated with increased values of lipid hydroperoxide, suggesting oxidative stress. RA also reduced citrate synthase, enzymatic mitochondrial complex II, ATP synthase, and enzymes of fatty acid metabolism and was associated with increased enzymes involved in glucose use. In addition, RA increased JNK 1/2 expression, without changes in TGF-β, PI3K, AKT, NFκB, S6K, and ERK. Conclusion: In normal rats, RA induces cardiac hypertrophy in a dose-dependent manner. The non-participation of the PI3K/Akt pathway, associated with the participation of the JNK pathway, oxidative stress, and changes in energy metabolism, suggests that cardiac remodeling induced by RA supplementation is deleterious. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-11-01 2018-12-11T17:15:24Z 2018-12-11T17:15:24Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1159/000481876 Cellular Physiology and Biochemistry, v. 43, n. 4, p. 1449-1459, 2017. 1421-9778 1015-8987 http://hdl.handle.net/11449/175341 10.1159/000481876 2-s2.0-85031409586 2-s2.0-85031409586.pdf |
url |
http://dx.doi.org/10.1159/000481876 http://hdl.handle.net/11449/175341 |
identifier_str_mv |
Cellular Physiology and Biochemistry, v. 43, n. 4, p. 1449-1459, 2017. 1421-9778 1015-8987 10.1159/000481876 2-s2.0-85031409586 2-s2.0-85031409586.pdf |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Cellular Physiology and Biochemistry 1,561 1,561 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1449-1459 application/pdf |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1799965660484206592 |