Effect of extracellular calcium on ciliary length in LLC-PK1 renal epithelial cells.

PEREZ PL; SCARINCI N; CANTERO MR; CANTIELLO HF

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

Polycystin-2 (PC2, TRPP2) is a Ca2+-permeable, nonselective cation channel whose dysfunction generates autosomal dominant polycystic kidney disease (ADPKD). PC2 is present in different cellular locations, including the primary cilium. The accepted hypothesis is that ADPKD is generated by changes in ciliary length, which is controlled by several proteins, chiefly among which is PC2. Previously we determined a functional PC2 in the primary cilium of LLC-PK1 cells, where it may contribute to Ca2+ transport. PC2 activation is also associated with a rise in cell Ca2+, instead associated with functional plasma membrane-located PC2 channels. Little is known, however, as to how renal epithelial cells control ciliary length, and in particular its regulation by extracellular Ca2+. Our most recent studies determined the presence of a feedback mechanism of PC2 function by the Calcium-Sensing Receptor, which is activated by extracellular Ca2+.