Törnquist K, Ekokoski E
Department of Zoology, University of Helsinki, Finland.
Biochem J. 1994 Apr 1;299 ( Pt 1)(Pt 1):213-8. doi: 10.1042/bj2990213.
The effects of sphingosine derivatives on Ca2+ fluxes were investigated in thyroid FRTL-5 cells labelled with Fura 2. Addition of sphingosylphosphocholine (SPC) or sphingosine (SP) increased intracellular free Ca2+ ([Ca2+]i) in a dose-dependent manner. At the highest dose tested (30 microM), the response was biphasic: a rapid transient increase in [Ca2+]i, followed by a new, elevated, level of [Ca2+]i. Both phases of the SPC-evoked increase in [Ca2+]i were dependent on extracellular Ca2+, whereas only the SP-evoked elevated level of [Ca2+]i was dependent on the influx of Ca2+. Both compounds released sequestered Ca2+ from thapsigargin- and inositol 1,4,5-trisphosphate (IP3)-sensitive Ca2+ pools. In addition, the increase in [Ca2+]i in response to SPC, but not to SP, was attenuated in cells treated with phorbol myristate acetate or with the putative Ca(2+)-channel blocker SKF 96365, and in cells pretreated with pertussis toxin for 24 h. SPC did not activate the production of IP3. Furthermore, both SPC and SP released sequestered Ca2+ from permeabilized cells. We observed that SPC, but not SP, stimulated release of [3H]arachidonate from cells prelabelled with [3H]arachidonate for 24 h. Both SPC and SP stimulated the incorporation of [3H]thymidine into DNA in cells grown in the absence of thyroid-stimulating hormone (TSH). The results suggest that sphingosine derivatives are putative regulators of Ca2+ fluxes in FRTL-5 cells, and that SP and SPC may act on [Ca2+]i via different mechanisms. Furthermore, both SP and SPC may be of importance in modulating thyroid-cell proliferation.
在以Fura 2标记的甲状腺FRTL-5细胞中研究了鞘氨醇衍生物对Ca2+通量的影响。添加鞘氨醇磷酸胆碱(SPC)或鞘氨醇(SP)会以剂量依赖的方式增加细胞内游离Ca2+([Ca2+]i)。在测试的最高剂量(30 microM)下,反应呈双相性:[Ca2+]i迅速短暂增加,随后是[Ca2+]i的新的升高水平。SPC引起的[Ca2+]i增加的两个阶段均依赖于细胞外Ca2+,而只有SP引起的[Ca2+]i升高水平依赖于Ca2+的流入。两种化合物都从毒胡萝卜素和肌醇1,4,5-三磷酸(IP3)敏感的Ca2+池中释放出被隔离的Ca2+。此外,在用佛波酯肉豆蔻酸酯或假定的Ca(2+)通道阻滞剂SKF 96365处理的细胞以及用百日咳毒素预处理24小时的细胞中,对SPC而非SP的反应中[Ca2+]i的增加减弱。SPC不会激活IP3的产生。此外,SPC和SP都从通透细胞中释放出被隔离的Ca2+。我们观察到,SPC而非SP刺激了预先用[3H]花生四烯酸标记24小时的细胞中[3H]花生四烯酸的释放。在无促甲状腺激素(TSH)生长的细胞中,SPC和SP都刺激了[3H]胸苷掺入DNA。结果表明,鞘氨醇衍生物可能是FRTL-5细胞中Ca2+通量的调节因子,并且SP和SPC可能通过不同机制作用于[Ca2+]i。此外,SP和SPC在调节甲状腺细胞增殖中可能都很重要。