RGD Reference Report - Redox regulation of myocardial ERK 1/2 phosphorylation in experimental hyperthyroidism: role of thioredoxin-peroxiredoxin system. - Rat Genome Database
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Redox regulation of myocardial ERK 1/2 phosphorylation in experimental hyperthyroidism: role of thioredoxin-peroxiredoxin system.

Authors: Araujo, AS  Fernandes, T  Ribeiro, MF  Khaper, N  Bello-Klein, A 
Citation: Araujo AS, etal., J Cardiovasc Pharmacol. 2010 Nov;56(5):513-7.
RGD ID: 5133711
Pubmed: (View Article at PubMed) PMID:20729758
DOI: Full-text: DOI:10.1097/FJC.0b013e3181f50a70

The present study was conducted to test whether adaptation in the antioxidant system would differentially modulate prosurvival and proapoptotic proteins in hyperthyroidism-induced cardiac hypertrophy. Male Wistar rats were divided into 4 groups: control, vitamin E (20 mg . kg(-1) . d(-1) subcutaneously, 28 days), thyroxine (T4) (12 mg/L in drinking water for 28 days), and T4 + vitamin E. Cardiac mass, redox ratio, glutathione peroxidase (GPx) and glutathione reductase (GR) activities, NF-E2-related factor 2 (Nrf2) thioredoxin-1 (Trx-1), peroxiredoxin-6 (Prx-6), phospho-extracellular-signal-regulated kinases 1/2 (p-ERK 1/2)/extracellular-signal-regulated kinases 1/2 (ERK1/2), and phospho-c-Jun N-terminal kinase (p-JNK)/c-Jun N-terminal kinase (JNK) myocardial protein expression were quantified. Cardiac hypertrophy was attenuated in the T4 + vitamin E group. The redox ratio; GPx and GR; as well as Nrf2, Trx-1, Prx-6, and p-ERK1/2/ERK1/2 immunocontent were elevated in T4 group. All these effects were attenuated by vitamin E administration. p-JNK/JNK remained unchanged in all the groups. The overall results suggest that redox imbalance due to hyperthyroidism induce adaptation of antioxidant systems, favoring ERK1/2 activation and leading to development of cardiac hypertrophy.

Annotation

Gene Ontology Annotations    

Biological Process

Objects Annotated

Genes (Rattus norvegicus)
Txn1  (thioredoxin 1)


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