PI3K signaling pathway is implicated in bradykinin-induced migratory phenotype of ureteric bud cells

GUAYTIMA EDITH; BRANDAN YAMILA; FAVALE NICOLAS; STERIN SPEZIALE NORMA; MARQUEZ M GABRIELA

Buenos Aires

Congreso; XLIX REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIONES BIOQUÍMICAS Y DE BIOLOGÍA MOLECULAR (SAIB); 2013

SOCIEDAD ARGENTINA DE INVESTIGACIONES BIOQUÍMICAS Y DE BIOLOGÍA MOLECULAR (SAIB)

In mammals, nephrogenesis is completed posnatally. We have previously shown that primary cultures of renal papillary ureteric bud (UB) cells of 7 days-old rats display a great capacity to form colonies, and interact with the substratum through focal adhesions (FA) immunostained with vinculin. Bradykinin (BK) treatment induces a migratory phenotype, and in some border cells, BK provokes a redistribution of vinculin from focal adhesion (FA) to the cytosol. In the present work, we tested whether PI3K signaling pathway was implicated in these phenomena. We observed that pre-treatment of cultured UB cells with the PI3K?specific inhibitor Ly294002, avoided BK?induced vinculin redistribution. We examined by immunofluorescence the cellular distribution of PI3K, PTEN, AKT and AKT-P in BK stimulated UB cells. PI3K immunostaining is located in the plasma membrane of border cells lacking FA but containing vinculin in the cytosol, and in the cytosol of cells containing FA. The same pattern of labeling was observed for AKT and AKT-P. Interestingly, cells containing FA do not express PTEN in the plasma membrane. We interpret that vinculin accumulation in the cytosol only occurs in those cells whose function is the one to indicate the direction of the collective migration of the UB cells, and PI3K signaling pathway is implicated in BK-induced migratory phenotype of these UB leader cells.