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1 Service of Nephrology, Fondation pour Recherches Medicales, Geneva, Switzerland
2 Department of Surgical Sciences, Karolinska Institutet, Stockholm, Sweden
3 INSERM U478, Faculte de Medecine Xavier Bichat, Paris, France
* To whom correspondence should be addressed. E-mail: Eric.Feraille{at}medecine.unige.ch.
In the renal collecting duct (CD), water reabsorption depends on the presence of aquaporin-2 (AQP2) in the apical membrane of principal cells. AQP2 expression and sub-cellular repartition is under the control of [8-arginine]vasopressin (AVP). Some pieces of experimental evidence indicate that additional hormonal factors, including insulin may also control AQP2 expression and thereby CD water permeability. We have previously shown that AVP induces endogenous AQP2 expression in cultured mouse mpkCCDcl4 collecting duct principal cells (23). In the present study, we investigated the effect of insulin on AQP2 expression in mpkCCDcl4 cells. Addition of insulin to the basal medium of cells grown on filters slightly increased AQP2 mRNA and protein expression while insulin potentiated the effect of AVP. The potentiation of AVP-induced AQP2 expression by insulin was abolished by actinomycin D, a transcriptional inhibitor. Analysis of AQP2 protein expression under conditions of AVP washout and/or in the presence of chloroquine, a lysosomal degradation inhibitor, revealed that insulin did not significantly alter AQP2 protein degradation. Inhibition of ERK, p38 kinase, and PI3-kinase activities prevented the insulin-induced stimulation of AQP2 expression, whereas inhibition of PKC has no effect. Taken together, our results indicate that insulin AQP2 protein expression mostly through increased AQP2 mRNA levels in cultured mpkCCDcl4 cells. This effect most likely relies on increased AQP2 gene transcription in response to MAPK and PI3-kinase activation.
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