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The Mediation of Aldosterone‐Induced Cortical Collecting Duct Cell Growth Through The Activation of Protein Kinase D1

Aldosterone elicits transcriptional and rapid signaling responses in target tissues such as the distal nephron. Aldosterone treatment of the M1 cortical collecting duct cell line (M1‐CCD) led to the stimulation of cell growth. This effect was protein kinase D1 (PKD1), PKCδ and ERK1/2‐dependent. Aldosterone induced the rapid activation of ERK1/2 with peaks of activation at 2 min and at 10 to 30 min after hormone treatment, followed by sustained ERK1/2 activation lasting beyond 120 min. M1‐CCD cells suppressed in PKD1 expression exhibited only the early, transient phase in ERK1/2 activation. Co‐immunoprecipitation experiments showed that aldosterone promoted the physical association of PKD1 with ERK1/2 within 2 min of treatment. The MR antagonist RU28318 inhibited the early and late phases of aldosterone‐induced ERK1/2 activation, and also the aldosterone‐induced cell growth. Aldosterone promoted the sub‐cellular redistribution of ERK1/2 to the nuclei of M1‐CCD cells after 2 min treatment and to sites, proximal to the nuclei after 30 min. The sub‐cellular redistribution of ERK1/2 was inhibited in PKD1 knock‐down cells. The stabilization of ERK1/2 activation by PKD1 and ERK1/2 cellular redistribution are a pre‐requisite for aldosterone‐induced cell growth. PKD1 activation by aldosterone may be an important factor in both renal differentiation and proliferative disease.