Elsevier

Peptides

Volume 16, Issue 6, 1995, Pages 1133-1140
Peptides

Article
Neuromedin B stimulates arachidonic acid release, c-fos gene expression, and the growth of C6 glioma cells

https://doi.org/10.1016/0196-9781(95)00085-XGet rights and content

Abstract

The effects of neuromedin B (NMB) on C6 glioma cells were investigated. NMB bound with high affinity (IC50 = 1 nM) to C6 cells whereas BN and GRP were less potent (IC50 = 40 and 100 nM). NMB (1 nM) elevated cytosolic Ca2+ in individual C6 cells and the increase in cytosolic Ca2+ was reversed by 1 μM [d-Arg1,d-Pro2,d-Trp7,9,Leu11]substance P [APTTL]SP, a broad spectrum antagonist. NMB stimulated [3H]arachidonic acid release from C6 cells and the increase in [3H]arachidonic acid release was reversed [APTTL]SP. NMB increased transiently c-fos gene expression in C6 cells. NMB increased the number of C6 colonies in soft agar and the increase in growth caused by NMB was reversed by [APITL]SP. These data suggest that NMB receptors may regulate the proliferation of C6 cells.

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      We discovered that a certain dose of NMB could significantly activate PKC, but there was no significant change in PKA, that means PKC signaling pathway may be activated. Previous studies have shown that NMB binding to its receptor can activate PKC in some cellular responses, then leading to the expression of related genes, DNA synthesis and/or cellular effects (Lach et al., 1995; Moody et al., 1995; Rozengurt, 1998, 2007; Sancho et al., 2011; Weber, 2009). These results suggest that NMB may regulate the testosterone synthesis via NMBR/PKC/steroidogenesis signaling pathway, but the specific mechanism of the regulation of the steroidogenesis by NMB/NMBR system needs further study in male rabbit.

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