N,N-dimethyl-D-erythro-sphingosine inhibits store-operated Ca[2+] entry in U937 monocytes

  • Jo Ji-Yeong
    Laboratory of Pharmacology, College of Pharmacy (BK21 Project) and Longevity Life Science and Technology Institutes, Pusan National University, Korea
  • Kim Hyo-Lim
    Laboratory of Pharmacology, College of Pharmacy (BK21 Project) and Longevity Life Science and Technology Institutes, Pusan National University, Korea
  • Lee Yun-Kyung
    Laboratory of Pharmacology, College of Pharmacy (BK21 Project) and Longevity Life Science and Technology Institutes, Pusan National University, Korea
  • Tomura Hideaki
    Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Japan
  • Bae Yoe-Sik
    Department of Biochemistry, College of Medicine, Dong-A University, Korea
  • Okajima Fumikazu
    Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Japan
  • Im Dong-Soon
    Laboratory of Pharmacology, College of Pharmacy (BK21 Project) and Longevity Life Science and Technology Institutes, Pusan National University, Korea

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  • N,N-Dimethyl-<sc>D</sc>-erythro-Sphingosine Inhibits Store-Operated Ca2+ Entry in U937 Monocytes

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Calcium is a ubiquitous second messenger that controls a broad range of cellular functions, and store-operated calcium entry (SOCE) is the primary mechanism of regulated Ca2+ entry in non-excitable immunocytes. In this study, we found that N,N-dimethyl-<sc>D</sc>-erythro-sphingosine (DMS) inhibited SOCE. In U937 cells, treatment with DMS for 2 h inhibited thapsigargin-induced SOCE by about 70%. DMS inhibited SOCE in a concentration-dependent manner when it was added to the cells after SOCE reached a plateau. DMS-induced SOCE inhibition was also confirmed by the Mn2+-quenching method, which monitors only Ca2+ influx. Because sphingosine kinase inhibitors or protein kinase C (PKC) inhibitors could not mimic the SOCE inhibition, sphingosine kinase and PKC could be excluded as targets of DMS-induced inhibition of SOCE. Furthermore, disruption of lipid rafts with methyl-β-cyclodextrin and bacterial sphingomyelinase did not influence DMS-induced inhibition of SOCE. DMS-induced inhibition of SOCE in U937 human monocytes is a unique observation and could serve as a basis to study modulation of intracellular Ca2+ concentration by sphingolipids, although the precise mechanism should be elucidated in the future.<br>

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