Increased expression of Galphaq protein in the heart of streptozotocin-induced diabetic rats
Experimental & Molecular Medicine
;
: 179-184, 1999.
Artículo
en Inglés
| WPRIM
| ID: wpr-158708
ABSTRACT
Heart disease is one of the major cause of death in diabetic patients, but the thogenesis of diabetic cardio-myopathy remains unclear. In this experiment, to sess the significance of G protein signaling pathways in the pathogenesis of abetic cardiomyopathy, we analyzed the expression of G proteins and the tivities of second messenger dependent protein kinases cAMP-dependent protein nase (PKA), DAG-mediated protein kinase C (PKC), and calmodulin dependent otein kinase II (CaM kinase II) in the streptozotocin induced diabetic rat art. The expression of Galphaq was increased by slightly over 10% (P<0.05) in abetic rat heart, while Galphas, Galphai, and Gbeta remained unchanged. The A activity in the heart did not change significantly but increased by 27%<0.01) in the liver. Insulin treatment did not restore the increased activity the liver. Total PKC activity in the heart was increased by 56% (P<0.01), and sulin treatment did not restore such increase. The CaM kinase II activity in e heart remained at the same level but was slightly increased in the liver 4% increase, P<0.05). These findings of increased expression of Galphaq in the reptozotocin-diabetic rat heart that are reflected by the increased level of C activity and insensitivity to insulin demonstrate that alteration of Galphaq y underlie, at least partly, the cardiac dysfunction that is associated with abetes. Copyright 2000 Academic Press.
Texto completo:
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Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Proteína Quinasa C
/
Transducción de Señal
/
Ratas Sprague-Dawley
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Estreptozocina
/
Proteínas Quinasas Dependientes de AMP Cíclico
/
Proteínas Quinasas Dependientes de Calcio-Calmodulina
/
Proteínas de Unión al GTP
/
Diabetes Mellitus Experimental
/
Insulina
/
Hígado
Límite:
Animales
Idioma:
Inglés
Revista:
Experimental & Molecular Medicine
Año:
1999
Tipo del documento:
Artículo
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