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Differential regulation of NaPi2a and NaPi2c by parathyroid hormone

2010; Wiley; Volume: 24; Issue: S1 Linguagem: Inglês

10.1096/fasebj.24.1_supplement.606.30

1530-6860

Kayo Okamura, Héctor Giral, Yupanqui Caldas, Eileen Sutherland, Andrew C. Millard, Moshe Levi, Judith Blaine,

Renal and related cancers

Parathyroid hormone (PTH) is a critical regulator of renal phosphate (Pi) homeostasis. In the kidney Pi reabsorption is regulated by the sodium phosphate cotransporters NaPi2a and NaPi2c. It has previously been shown that PTH‐induced removal of NaPi2c from the renal proximal tubule brush border membrane (BBM) is approximately 3 times slower than that of NaPi2a. The reason for this is unknown. Using a novel application of total internal reflection fluorescence microscopy (TIR‐FM) to the apical membrane of renal proximal tubule cells we have found that a dynamic actin cytoskeleton and the unconventional myosin motor myosin VI are required for PTH induced removal of NaPi2a from the BBM. Here we demonstrate that a dynamic actin cytoskeleton is required for NaPi2c removal from the BBM in response to PTH. In addition we investigate the role of myosin VI and membrane lipid dynamics in PTH‐induced trafficking of NaPi2c. Differences in the use of motor proteins or clustering of the cotransporters within the BBM may account for the differences in the kinetics of the response of NaPi2a and NaPi2c to PTH. Supported by NIH K08 DK080989‐01A1 .