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  • Title: Lipopolysaccharide regulates both serotonin- and thrombin-induced intracellular calcium mobilization in rat C6 glioma cells: possible involvement of nitric oxide synthase-mediated pathway.
    Author: Tawara Y, Kagaya A, Uchitomi Y, Horiguchi J, Yamawaki S.
    Journal: J Neurosci Res; 1998 Feb 15; 51(4):517-25. PubMed ID: 9514205.
    Abstract:
    To investigate the mechanisms by which lipopolysaccharide (LPS) affects Ca2+ signaling systems, we studied the effects of LPS on the serotonin (5-HT)- or thrombin-induced intracellular Ca2+ ([Ca2+]i) increase in rat C6 glioma cells. Pretreatment of the cells with 1 microg/ml LPS for 24 hr significantly inhibited [Ca2+]i increase induced by 10 microM 5-HT- or 0.5 U/ml thrombin. Its inhibitory effects were both dose- and time-dependent. Treatment with 1 mM dibutyryl cGMP (dbcGMP) for 30 min also significantly inhibited the 5-HT- and thrombin-induced [Ca2+]i increase to approximately 60-70% of control. However, simultaneous pretreatment with LPS and dbcGMP did not show any synergistic inhibition. The simultaneous pretreatment with LPS and the potent cGMP-dependent protein kinase (PKG) inhibitors H-8 and KT5823 for 24 hr significantly antagonized the inhibitory effect of LPS. Pretreatment of the cells with 1 microg/ml LPS for 24 hr significantly enhanced cGMP accumulation, while dexamethasone and NMMA (NOS inhibitors) significantly attenuated the LPS-induced enhancement in cGMP accumulation. In addition, pretreatment of the cells with 100 nM dexamethasone for 24 hr significantly suppressed LPS-induced inducible nitric oxide synthase (iNOS; type II NOS, NOS-II) protein expression. These results indicate that LPS may inhibit both 5-HT- and thrombin-induced [Ca2+]i increase via iNOS expression and PKG activation pathway in rat C6 glioma cells.
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