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Objective: Inherited Polycystic kidney disease has been linked to defects in cilial function of renal epithelial cells. Cilial bending in vitro through mechanical stimulation or flow has been shown to result in an increase in intracellular calcium, which is polycystin-1 and polycystin-2 dependent. The present experiments aimed at imaging downstream signalling events in MDCK cells by time lapse imaging. Methods: A parallel plate chamber was designed for life cell imaging under flow conditions. Ciliated MDCK cells and nonciliated control cells were imaged under different flow conditions and increase of intracellular calcium was determined by fura-2 ratio imaging. Virally transduced MDCK cells expressing a Protein Kinase C (PKC) gamma-GFP fusion construct, or a deletion construct with the C2 domain fused to GFP, were examined under flow conditions and the subcellular localization of PKC was tracked by time lapse imaging. Results: Intracellular calcium increased in wild type MDCK cells in response to flow in cilated cells only, when compared with non ciliated control cells. Ciliated MDCK cells expressing PKC-GFP or C2-GFP showed translocation of PKC to the plasma membrane in response to flow. Translocation of C2-GFP was enhanced, when compared to full length GFP, as would be expected in the absence of the C1 domains. Conclusions: The increase in intracellular calcium in renal epithelial cells in response to cilial bending is associated with the translocation of Protein Kinase C to the plasma membrane. Further studies will attempt to identify targets of downstream signalling of PKC. [ABSTRACT FROM AUTHOR]