1,25-二羟维生素D-3通过特定血小板活化因子（PAF）结合位点的表达增强PAF刺激的U937细胞钙动员。

1,25-(OH)2 vitamin D-3 enhances Paf-stimulated calcium mobilization in U937 cells by expression of specific Paf binding sites.

作者信息

Aepfelbacher M, Korth R, Weber P C

机构信息

Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Universität München, F.R.G.

出版信息

Biochim Biophys Acta. 1990 Feb 19;1051(2):179-84. doi: 10.1016/0167-4889(90)90191-f.

DOI:10.1016/0167-4889(90)90191-f

PMID:2155666

Abstract

The effect of 1,25-(OH)2 vitamin D-3 (10 nM, 72 h) on cytosolic free Ca2+ concentration ([Ca2+]i) in U937 cells before and after stimulation with Paf, LTD4 and ADP was investigated. 1,25-(OH)2 vitamin D-3 increased basal [Ca2+]i from 98 +/- 1 nM to 121 +/- 5 nM (P less than 0.01) and the Paf (10 nM) stimulated increase in [Ca2+]i from 143 +/- 15 to 406 +/- 44 nM (P less than 0.01). These vitamin D-3 effects were time-related and occurred after 24 h (basal [Ca2+]i) and 12 h (Paf stimulated Ca2(+)-mobilization) but not after 3 h. In comparison, vitamin D-3 failed to modulate Ca2(+)-mobilization in response to ADP (1-40 microM) and increased it only in response to low leukotriene D4 concentrations (0.1-1 nM). The total binding of [3H]Paf (2.8 nM) was not significantly different in untreated vs. vitamin D-3-treated cells. However, the Paf receptor antagonist Web 2086 (1 microM) inhibited [3H]Paf binding only in vitamin D-3-treated cells. The specific binding reached a plateau of 28 +/- 3 fmol per 2.5.10(6) cells between 1.4 and 2.8 nM [3H]Paf. The Paf receptor antagonist Web 2086 (1-1000 nM) also inhibited the Paf-mediated Ca2(+)-mobilization in vitamin D-3-treated cells (IC50 = 191 +/- 55 M). These data suggest that the enhanced Ca2(+)-mobilization in vitamin D-3-treated U937 cells in response to Paf is mediated by an expression of putative Paf receptors.

摘要

研究了1,25-(OH)2维生素D-3（10 nM，72小时）对U937细胞在用血小板活化因子（Paf）、白三烯D4（LTD4）和二磷酸腺苷（ADP）刺激前后胞质游离钙离子浓度（[Ca2+]i）的影响。1,25-(OH)2维生素D-3使基础[Ca2+]i从98±1 nM升高至121±5 nM（P<0.01），并使Paf（10 nM）刺激的[Ca2+]i升高从143±15 nM升至406±44 nM（P<0.01）。这些维生素D-3的作用与时间相关，在24小时（基础[Ca2+]i）和12小时（Paf刺激的Ca2+动员）后出现，但3小时后未出现。相比之下，维生素D-3未能调节对ADP（1 - 40 μM）的Ca2+动员，仅对低浓度白三烯D4（0.1 - 1 nM）有增加作用。未处理细胞与维生素D-3处理细胞中[3H]Paf（2.8 nM）的总结合无显著差异。然而，Paf受体拮抗剂Web 2086（1 μM）仅在维生素D-3处理的细胞中抑制[3H]Paf结合。在1.4至2.8 nM [3H]Paf之间，每2.5×10(6)个细胞的特异性结合达到28±3 fmol的平台期。Paf受体拮抗剂Web 2086（1 - 1000 nM）也抑制维生素D-3处理细胞中Paf介导的Ca2+动员（IC50 = 191±55 nM）。这些数据表明，维生素D-3处理的U937细胞中对Paf反应增强的Ca2+动员是由假定的Paf受体表达介导的。