Pandol S J, Schoeffield-Payne M S, Gukovskaya A S, Rutherford R E
Department of Veterans Affairs Medical Center, San Diego, CA 92161.
Biochim Biophys Acta. 1994 Oct 12;1195(1):45-50. doi: 10.1016/0005-2736(94)90007-8.
The purpose of present study was to examine the effects of sphingosine on cellular Ca2+ transports using dispersed rat pancreatic acini. The results demonstrated that sphingosine had a specific effect to inhibit Ca2+ uptake into the cell's agonist-sensitive pool as well as inhibiting microsomal Ca(2+)-ATPase. The ability of sphingosine to inhibit Ca2+ uptake resulted in both augmentation of Ca2+ release from the pool by inositol 1,4,5-trisphosphate (IP3) and conversion of the Ca2+ release by inositol 1,4,5-trisphosphate from a transient response to a sustained response. Furthermore, by preventing Ca2+ pool refilling sphingosine mimicked the effect of the agonist, carbachol, to maintain an increased [Ca2+]i during sustained stimulation. These results suggest that regulation of Ca(2+)-ATPase by sphingosine or a sphingosine-like agent mediates some of the effects of agonist on cell Ca2+ transports.
本研究的目的是利用分散的大鼠胰腺腺泡来检测鞘氨醇对细胞钙转运的影响。结果表明,鞘氨醇具有特异性作用,可抑制钙离子摄取进入细胞的激动剂敏感池,同时抑制微粒体钙-ATP酶。鞘氨醇抑制钙离子摄取的能力导致肌醇1,4,5-三磷酸(IP3)引起的钙池释放增加,以及肌醇1,4,5-三磷酸引起的钙释放从瞬时反应转变为持续反应。此外,通过阻止钙池再填充,鞘氨醇模拟了激动剂卡巴胆碱的作用,以在持续刺激期间维持细胞内钙离子浓度升高。这些结果表明,鞘氨醇或类似鞘氨醇的物质对钙-ATP酶的调节介导了激动剂对细胞钙转运的一些影响。