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Redox status and pro‐survival/pro‐apoptotic protein expression in the early cardiac hypertrophy induced by experimental hyperthyroidism
Author(s) -
Fernandes R. O.,
Dreher G. J.,
Schenkel P. C.,
Fernandes T. R. G.,
Ribeiro M. F. M.,
Araujo A. S. R.,
BellóKlein A.
Publication year - 2011
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1796
Subject(s) - thioredoxin , protein kinase b , medicine , endocrinology , glutathione , mapk/erk pathway , muscle hypertrophy , redox , thioredoxin reductase , western blot , chemistry , protein kinase a , apoptosis , oxidative stress , biology , kinase , biochemistry , enzyme , organic chemistry , gene
This study was conducted to analyse the redox status and redox‐sensitive proteins that may contribute to a non‐genomic mechanism of cardiac hypertrophy induction by hyperthyroidism. Wistar rats, treated with L‐thyroxine (T4) during 2 weeks (12 mg·l ‐1 in drinking water), presented cardiac hypertrophy (68% higher than control), without signals of liver or lung congestion. Myocardial reduction of the reduced glutathione: oxidized glutathione (GSSG) ratio (45%) (redox status) and elevation in hydrogen peroxide concentration (H 2 O 2 ) (28%) were observed in hyperthyroid as compared with the control. No significant difference was found in thioredoxin (Trx), Trx reductase activity and Nrf2 (a transcriptional factor) protein expression between groups. Redox‐sensitive proteins, quantified using Western blot, presented the following results: increased p‐ERK: total extracellular‐regulated kinase (ERK) (200%) and Bax : Bcl‐2 (62%) ratios and reduced total‐Akt (63%) and p‐Akt (53%) expressions in the hyperthyroid rats as compared with the control. The redox imbalance, associated with increased immunocontent of a protein related to maladaptative growth (ERK) and reduced immunocontent of protein related to cytoprotection/survival (Akt), may suggest that the molecular scenario could favour the decompensation process of cardiac hypertrophy induced by experimental hyperthyroidism. Copyright © 2011 John Wiley & Sons, Ltd.