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The correlation of redox‐sensitive proapoptotic proteins and thioredoxin in early and late post‐infarction cardiac remodeling
Author(s) -
Schenkel Paulo Cavalheiro,
Tavares Angela,
Fernandes Rafael,
Diniz Gabriela,
Ribeiro Maria,
Araujo Alex,
BarretoChaves Maria Luiza,
BellóKlein Adriane
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1094.8
Subject(s) - thioredoxin , ventricular remodeling , redox , cardiology , myocardial infarction , medicine , microbiology and biotechnology , chemistry , oxidative stress , biology , organic chemistry
In this study, we investigated the correlation between thioredoxin‐1 (Trx‐1), renin‐angiotensin system (RAS) and hydrogen peroxide (H 2 O 2 ) concentration and their associations in some prosurvivaland proapoptotic proteins during early and late cardiac remodeling (CR) post myocardial infarction (MI). Male Wistar rats (±60 days) were divided into 6 groups: 3 sham‐operated (Sham) and 3 (MI): 2 days, 7 days and 28 post surgical procedure. Cardiac function was analyzed by echocardiography and, still under anesthesia, the animals were killed by cervical dislocation and the heart prepared for biochemical analysis. Our results show that Trx‐1 appears to be important to keep H 2 O 2 at low concentrations and avoid the activation of some proapoptotic proteins in early CR post‐MI. However, Trx‐1 decreases over 28 days post‐MI and this finding is associated with an increase in the RAS, when there is targeting to cell death and ventricular dysfunction. Taken together, our results suggest an inability of Trx‐1 in counterregulated the formation of additional reactive oxygen species promoted by increased activation of the RAS. This scenario seems to be favorable to the cardiac dysfunction post‐MI.