Adenosine triphosphate affects interleukin -1beta release by T98G glioblastoma cells through a purinoceptor-independent mechanism.

T98G glioblastoma cells were previously shown to significantly increase interleukin-1beta (IL-1beta) mRNA levels in response to IL-1beta stimulation. This work demonstrates that in such conditions T98G, despite possessing biologically active interleukin converting enzyme, do not release detectable amounts of IL-1beta, even in the presence of 20 mM adenosine triphosphate (ATP). IL-1beta secretion is observed only following concomitant stimulation with 1000 units/ml of IL-1beta and 20 mM ATP. ATP induces a dose-dependent depolarization of T98G plasma membrane, whereas it does not affect Ca(2+) concentration or cell membrane permeability. Our data, together with the observation that the depolarizing effects of ATP are retained after preincubation with 100 microM suramin, an antagonist of P2-purinoceptors, suggest that ATP plays a role in IL-1beta secretion by T98G but its effects do not occur through P2-purinoceptors.