The retinal pigment epithelium (RPE) is involved in a variety of processes that help to maintain normal retinal function. Many of these tasks depend on intracellular free calcium ([Ca2+ ]i), for example photoreceptor phagocytosis, growth factor secretion, transepithelial transport mechanisms and cell differentiation. The purpose of this study was to identify the molecular identity of Ca2+ channels involved in basal Ca2+ entry in RPE cells.

ARPE-19 cells had an resting [Ca2+ ]i of 106.4 ± 16.1 nM. This resting concentration was not changed by the application of the voltage-gated Ca2+ channel blocker nifedipin (10 mM). Gadolinium (100 mM); lanthanum (100 mM) and nickel (2 mM) reduced the [Ca2+ ]i by 73, 76 and 98%, respectively. Additionally, the blocker of store-operated Ca2+ entry 2- aminoethoxydiphenyl borate (75 mM) reduced [Ca 2+ ]i by 69%. As these blockers are known to block Ca2+ conducting channels of the TRPC family we performed RT PCR experiments and found TRPC1 and TRPC4 to be expressed in ARPE-19 cells. In freshly isolated RPE cells TRPC7 was expressed in addition to TRPC1 and TRPC4.

Our data show that the basal Ca2+ entry in RPE cells is mainly driven by TRPC1 and TRPC4 channels. Their basal open probability provides the basal [Ca2+ ]i needed for the function of diverse Ca2+ -dependent processes in RPE cells.