INVESTIGADORES
HONORE Stella Maris
congresos y reuniones científicas
Título:
Experimental diabetes alters cell-cell contacts in intestinal smooth muscle layer.
Autor/es:
HONORÉ S. M.; ZELARAYÁN L. C.; GENTA S. B.; VILLECCO E. I.; SÁNCHEZ S. S.
Lugar:
Mar del Plata, Buenos Aires. Argentina.
Reunión:
Congreso; XLIII Annual Meeting of the Argentine Society for Biochemistry and Molecular Biology (SAIB); 2007
Institución organizadora:
Society for Biochemistry and Molecular Biology (SAIB)
Resumen:
Intestinal dysfunction is one of the clinical complication of Diabetes. In this regard, the smooth muscle layer of the intestine has a critical role in motility. However, the detailed molecular mechanisms of intestinal motility dysfunction in diabetes remain unclear. In diabetes altered intercellular communications may account for some aspects of the enhanced contraction and/or impaired relaxation of muscular layer observed in the intestine and a consequently, result in the disturbed motility. To better understand the impact of diabetes on muscle layer dysfunction, we analyzed gap junctions and the N-cadherin/â-catenin complex in an experimental model of diabetes in rodents. Jejunum samples from normal and diabetic animals were analyzed by RT-PCR, immunohistochemistry, Western-immunoblotting and confocal microscopy in order to determine the expression of the junctions. Our results show a decrease in Conexin 43 (Cx43) expression in the muscle layer between smooth muscle cells during diabetes. Studies of colocalization of Cxs and c-kit showed that Cx43 localization in the intersticial cell of Cajal (ICC) network remained unchanged. In contrast, Cx45 showed a strong cytoplasmic reactivity in the myenteric plexus cells in diseased animals compared to controls. Diabetic injury produced a significantly reduction in the N-cadherin/â-catenin complex. The alterations in the gap junctions and N-cadherin/â-catenin complex observed in the diabetic rodent intestine suggest an impaired intercellular communication between the cells of the muscle layer and may be partially responsible for motility dysfunction.
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