TY - JOUR AU - HAN Jian-zhong AU - LIN Wen AU - CHEN Yi-zhang PY - 2016 TI - Inhibition of ATP-induced calcium influx in HT4 cells by glucocorticoids: involvement of protein kinase A JF - Acta Pharmacologica Sinica; Vol 26, No 2 (February 2005): Acta Pharmacologica Sinica Y2 - 2016 KW - N2 - Aim: In our previous observations, adenosine triphosphate (ATP) was found to evoke immediate elevations in intracellular free calcium concentration ([Ca 2+ ] i ) in HT4 neuroblastoma cells of mice. We tried to see if a brief pretreatment of glucocorticoids could inhibit the Ca 2+ response and reveal the underlying signaling mechanism. Methods: Measurement of [Ca 2+ ] i was carried out using the dual-wavelength fluorescence method with Fura-2 as the indicator. Results: Preincubation of HT4 cells for 5 min with corticosterone (B) or bovine serum albumin conjugated corticosterone (B-BSA) inhibited the peak [Ca 2+ ] i increments in a concentration-dependent manner. Cortisol and dexamethasone had a similar action, while deoxycorticosterone and cholesterol were ineffective. Both extracellular Ca 2+ influx and internal Ca 2+ release contributed to ATP-induced [Ca 2+ ] i elevation. The brief treatment with only B attenuated Ca 2+ influx. Furthermore, the [Ca 2+ ] i elevation induced by the P2X receptor agonist adenosine 5’-(β,γ-methylene) triphosphate (β,γ-meATP) was also suppressed. The rapid inhibitory effect of B can be reproduced by forskolin 1 mmol/L and blocked by H89 20 mmol/L. Neither nuclear glucocorticoid receptor antagonist mifepristone nor protein kinase C inhibitors influenced the rapid action of B. Conclusion: Our results suggest that glucocorticoids modulate P2X receptor-medicated Ca 2+ influx through a membrane- initiated, non-genomic and PKA-dependent pathway in HT4 cells. UR - http://www.chinaphar.com/article/view/3548