SANCHEZ Sara Serafina Del V.
congresos y reuniones científicas
Down regulation of GAP junctions and Cadherin-beta Catenin complexes in diabetic small intestine.
HONORÉ S.M.; ZELARAYÁN L.C.; GENTA S.B.; VILLECCO E.I.; SÁNCHEZ S.S.
Carlos Paz, Córdoba, Argentina
Congreso; XLIV Annual Meeting of the Argentine Society for Biochemistry and Molecular Biology (SAIB); 2008
Diabetes mellitus is associated with long-term damage of the gastrointestinal tract.To better understand the impact of hyperglycemia on intestinal intercellular communications, we analyzed the expression of gap junctions (GJ) and cadherin/â-catenin complex in an experimental model of diabetes in rodents. High glucose down-regulated junctions in the mucosa and muscle layers of the intestine at early stages of the disease. Reduced expression of Cx43 and Cx45 proteins and aberrant cytoplasmic localization was determined in the mucosa layer and in the myenteric plexus cells. Results indicated that diabetes produced a Cx43 dephosphorilation. This could lead to an intracytoplasmic localization of this protein with a consequent loss of functional form. In the muscle layer the decreased in gap junction intercellular communication between smooth muscle cells exposed to high glucose was associated with a loss of Cx43 from the plasma membrane, as demonstrated by immunohistochemistry. Functional GJ requires appropriate cell adhesion mediated by the cadherin/â-catenin complex. Diabetic injury produced a significantly reduction in the cadherin/â-catenin complex contributing to abnormal intestinal cell-cell interactions. We propose that altered junctional adhesion molecules play a significant role at early stages of diabetic intestinal pathogenesis.