Depolarisation induces rapid and transient formation of intracellular sphingosine-1-phosphate
| Autor: | Holger Lass, Karl Jakobs, Burkhard Kleuser, Regina Alemany, Lars Ruwisch, Dagmar Meyer zu Heringdorf, Rozita Hashemi, Sarah Spiegel, Kerstin Danneberg |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Sphingosine-1-phosphate
Biophysics Sphingosine kinase Bradykinin Biology Biochemistry PC12 Cells Potassium Chloride chemistry.chemical_compound Norepinephrine Structural Biology Cell surface receptor Sphingosine Genetics Extracellular Animals Calcium Signaling Molecular Biology PC12 cell KCl depolarisation Cell Membrane Depolarization Cell Biology Hedgehog signaling pathway Recombinant Proteins Cell biology Rats Phosphotransferases (Alcohol Group Acceptor) chemistry Verapamil Noradrenaline release Calcium Channels Lysophospholipids Intracellular |
| Zdroj: | FEBS letters. 509(2) |
| ISSN: | 0014-5793 |
| Popis: | Formation of sphingosine-1-phosphate (SPP) by sphingosine kinase serves as a signalling pathway for various membrane receptors. Here, we show that membrane depolarisation is another mechanism by which this pathway can be activated. Formation of [(3)H]SPP as well as levels of endogenous SPP were rapidly and transiently increased in PC12 pheochromocytoma cells depolarised with high KCl. Time course and maximum were similar to those induced by bradykinin. Depolarisation-induced SPP production was also observed in RINm5F insulinoma cells, dependent on extracellular Ca(2+) and fully suppressed by verapamil, thus apparently caused by Ca(2+) influx via voltage-gated Ca(2+) channels. Studies with sphingosine kinase inhibitors and overexpression of sphingosine kinase revealed a partial contribution of this pathway to depolarisation-induced noradrenaline release and Ca(2+) increase. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text