Journal
CELLULAR AND MOLECULAR NEUROBIOLOGY
Volume 26, Issue 3, Pages 237-246Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-006-9016-1
Keywords
FGF-1; S100A13; Ca(2+)influx; voltage-dependent N-type Ca(2+)channel; amlexanox; omega-conotoxin; FRET; NG108-15 cells; non-vesicular release
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1. The Ca2+-mediated regulation of interaction between FGF-1 and S100A13 in NG108-15 cells was studied. When the stress by depriving B27 supplement from the culture was given, cellular levels of both proteins were decreased, while their releases were significantly increased within 3 h. These stress-induced changes were all abolished by amlexanox, an anti-allergic drug. 2. These releases were significantly inhibited by the addition of EGTA or BAPTA-AM, cellular or extracellular Ca2+-chelating agent, respectively. The addition of omega-conotoxin GVIA, a N-type Ca2+-channel blocker caused a complete inhibition of the release, while increased the cytosolic levels of both proteins. However, omega-conotoxin MVIIC, the non-N-type Ca2+-channel blocker was ineffective. 3. In NG108-15 cells, which had been transfected with Venus-FGF-1 and CFP-S100A13, the supplement-deprivation stress caused several spike-type fluorescence resonance energy transfer (FRET) signals, suggesting that both proteins showing interaction would be immediately released. These spikes were completely abolished by the addition of omega-conotoxin GVIA. However, the addition of amlexanox caused bell-shaped FRET signals without spikes. 4. Thus, it is suggested that the interaction between FGF-1 and S100A13 responsible for stress-induced non-vesicular release is dependent of Ca2+-influx through N-type Ca2+-channels.
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