MITOCHONDRIAL PROTEIN EXPRESSION IN NATURAL AND INDUCED FORMS OF CANINE DILATED CARDIOMYOPATHY

AUTOR(ES)

Rosana Lopes

FONTE

IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia

DATA DE PUBLICAÇÃO

2005

RESUMO

Idiopathic dilated cardiomyopathy (DCM) is now widely regarded as a syndrome in which a variety of etiological and predisposing factors give rise to myocardial dysfunction ultimately reflected in a similar pathological condition. DCM is the most well-known myocardial disease in dogs characterized by ventricular dilation and diminished cardiac function. The pathogenic mechanisms underlying cardiac disease are still largely unknown. However, in humans, mitochondriocytopathies have been associated to myocardial diseases. The mitochondrion is responsible for several essential processes in the heart such as energy metabolism, antioxidant biosynthesis, calcium homeostasis and programmed cell death. It is likely though, that significant alterations in myocardial physiology underlie these disease processes and determine their progression and outcome. The understanding of mitochondrial protein expression in dogs with idiopathic DCM could unveil important pathophysiological mechanisms associated with disease cause and progression. To better understand the biochemical mechanisms of idiopathic DCM in human beings, experimental models of congestive heart failure (CHF) have been employed. Dogs subjected to rapid ventricular pacing have been utilized to anticipate and understand the myocardial dysfunction in humans. In this study, qualitative and quantitative differences in canine heart mitochondrial protein expression were evaluated between control dogs, and dogs with idiopathic or DCM induced by rapid ventricular pacing. The most affected group of mitochondrial proteins was associated with energy metabolism. The myocardium depends on mitochondria for energy production. About 90% of energy in the heart is metabolized by mitochondria through the oxidative phosphorylation process. In addition mitochondrial proteins associated with primary energy, antioxidant defense and metabolism were significantly changed. Interestingly, altered mitochondrial protein expression patterns in the acquired form of DCM differed from those associated with experimentally-induced DCM. In conclusion, mitochondrial proteins associated with essential metabolic pathways were found to be altered in the myocardium of dogs with DCM. The altered mitochondrial proteins were mainly related to oxidative phosphorylation, but also included other elements of primary energy and other types of metabolism, antioxidant defense and programmed cell death. Maladjustment in proteins associated to energy likely indirectly reflect changes in other biological processes in myocardium.

ASSUNTO(S)

clinica veterinaria canine dilated cardiomyopathy dogs - myocardial disease

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