Sphingosine kinase-mediated Ca2+ signalling by G-protein-coupled receptors

The EMBO Journal (1998) 17, 2830–2837, doi:10.1093/emboj/17.10.2830

Table 2

Sphingosine kinase-mediated Ca²⁺ signalling by G-protein-coupled receptors

Dagmar Meyer zu Heringdorf, Holger Lass, Regina Alemany, Kai T. Laser, Eva Neumann, Chunyi Zhang, Martina Schmidt, Ursula Rauen, Karl H. Jakobs and Chris J. van Koppen

Table 2: Effect of DHS on [Ca²⁺]_i increases by various G-protein-coupled receptors

Cell type	Thrombin		LPA		Bradykinin
Cell type
Control (nM)	DHS (%)	Control (nM)	DHS (%)	Control (nM)	DHS (%)
HEK-293	46935	569^a	33755	3814^a	n.d.
J82	679	8212	61523	346^a	43036	407^a
OK	n.d.		46936	418^a	2997	355^a
BAEC	n.d.		n.d.		291124	1022^b

Following pretreatment with vehicle (Control) or 30 M DHS for 10 min, agonist-induced [Ca²⁺]_i increases were determined by measuring fura-2 fluorescence in HEK-293 cells, J82 transitional-cell carcinoma cells, opossum kidney cells (OK) and bovine aortic endothelial cells (BAEC). Peak [Ca²⁺]_i increases in control cells (in nM) and DHS-treated cells (as a percentage of those in control cells) are the meanSEM of 4–13 experiments. Concentrations applied were 1 U/ml thrombin, 1 M lysophosphatidic acid (LPA) and 1 M bradykinin. ^a[Ca²⁺]_i increase is significantly inhibited by DHS pretreatment (p<0.05, t-test). ^bEven at lower concentrations of bradykinin (0.1–100 nM), no influence of DHS was apparent. n.d., not determined.


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