IFIBIO HOUSSAY   25014
INSTITUTO DE FISIOLOGIA Y BIOFISICA BERNARDO HOUSSAY
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
AQP2-increased renal cell proliferation involves the activation of a NHE2-regulatory volume increase mechanism
Autor/es:
DI GIUSTO G; FORD P; CAPURRO C; RIVAROLA V
Lugar:
Foz de Iguazu
Reunión:
Congreso; 1st PanAmerican Congress of Physiological Sciences; 2014
Institución organizadora:
Asociación Latinoamericana de Ciencias Fisiológicas
Resumen:
We have previously shown in renal cells that expression of Aquaporin 2 (AQP2) induces cell cycle acceleration by shortening the transit time through S and G2 phases. Part of this acceleration is due to a down-regulation of regulatory volume decrease mechanism (RVD) in order to increase cell volume to proceed into S phase. We hypothesize that a regulatory volume increase mechanism (RVI) may also be activated. In this study we investigated if the isoform 2 of the Na+/H+ exchanger (NHE2), main responsible of RVI, contributed to the AQP2-increased proliferation. Two cortical collecting duct cell lines were used: WT-RCCD1 (not expressing AQPs) and AQP2-RCCD1 (transfected with AQP2). Unsynchronized (mostly in G1) or S phase-synchronized cells were used. Studies of intracellular pH, cell cycle kinetics, cell volume, immunoblot and immunofluorescence were performed. Results showed that NHE2 activity and expression were increased in AQP2-expressing cells. In these cells, NHE2 inhibition decreased cell proliferation and delayed cell cycle by slowing S and G2 phases. We also observed that only in AQP2-expressing cells a NHE2-dependent RVI machinery was activated in the S phase. Together these results suggest that the AQP2-dependent increased proliferation may be due in part to the activation of a RVI mechanism dependent on NHE2. Therefore, during cell cycle, a coordinated modulation of the RVD/RVI activity would contribute to accelerate proliferation of AQP2-expressing cells.