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Discriminating between Capacitative and Arachidonate-activated Ca2+ Entry Pathways in HEK293 Cells*

T. Shuttleworth,Jill L. Thompson

Published 1999 in Journal of Biological Chemistry

ABSTRACT

We have recently questioned whether the capacitative or store-operated model for receptor-activated Ca2+ entry can account for the influx of Ca2+ seen at low agonist concentrations, such a those typically producing [Ca2+] i oscillations. Instead, we have identified an arachidonic acid-regulated, noncapacitative Ca2+ entry mechanism that appears to be specifically responsible for the receptor-activated entry of Ca2+ under these conditions. However, it is unclear whether these two systems reflect the activity of distinct entry pathways or simply different mechanisms of regulating a common pathway. We therefore used the known selectivity of the Ca2+-stimulated type VIII adenylyl cyclase for Ca2+ entry occurring via the capacitative pathway (Fagan, K. A., Mahey, R., and Cooper, D. M. F. (1996)J. Biol. Chem. 271, 12438–12444) to attempt to discriminate between these two entry mechanisms in HEK293 cells. Consistent with the earlier reports, we found that thapsigargin induced an approximate 3-fold increase in adenylyl cyclase activity that was unrelated to global changes in [Ca2+] i or to the release of Ca2+ from internal stores but was specifically dependent on the induced capacitative entry of Ca2+. In marked contrast, the arachidonate-induced entry of Ca2+ completely failed to affect adenylyl cyclase activity despite producing a substantially greater rate of entry than that induced by thapsigargin. These data demonstrate that the arachidonate-activated entry of Ca2+occurs via an entirely distinct influx pathway.

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