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Related Experiment Video

Updated: May 14, 2026

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry

Published on: October 28, 2014

Intracellular calcium release modulates polycystin-2 trafficking.

Ayako Miyakawa¹, Cristián Ibarra, Seth Malmersjö

¹Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77, Stockholm, Sweden.

|February 13, 2013

Summary

Polycystin-2 (PC2) moves to the plasma membrane in kidney cells when calcium signaling is activated. This calcium-dependent trafficking may explain cyst formation in autosomal dominant polycystic kidney disease (ADPKD).

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Published on: September 1, 2015

Area of Science:

Nephrology
Cell Biology
Molecular Biology

Background:

Polycystin-2 (PC2) is an ion channel implicated in autosomal dominant polycystic kidney disease (ADPKD).
The precise subcellular localization and signaling roles of PC2 in kidney cells remain debated.

Purpose of the Study:

To investigate the dynamic subcellular localization of PC2 in kidney cells.
To determine the role of intracellular calcium (Ca2+) signaling in PC2 trafficking.

Main Methods:

Immunocytochemistry and confocal microscopy were used to track PC2 localization in primary human and rat proximal tubule cells.
Plasma membrane (PM) Ca2+ permeability was assessed using Fura-2 manganese quenching and time-lapse fluorescence microscopy.

Main Results:

PC2 displayed a dynamic distribution, shifting from the cytosol/reticulum to the PM upon stimulation of Ca2+ signaling pathways.
Ouabain treatment induced PC2 translocation to the PM and increased PM Ca2+ permeability.
Inhibition of Ca2+ signaling pathways (e.g., BAPTA, 2-APB, KN-93) blocked ouabain-stimulated PC2 PM translocation.

Conclusions:

PC2 undergoes intracellular Ca2+-dependent trafficking in kidney cells.
This Ca2+-dependent PC2 movement may offer new insights into the pathogenesis of ADPKD cystogenesis.