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Capacitative Ca2+ entry involves Ca2+ influx factor in rat glioma C6 cells
1Department of Pharmacology, School of Medicine, Sapporo Medical University, Japan.
Life Sciences
|June 3, 1999
Summary
Calcium influx factor (CIF) triggers capacitative calcium entry in rat glioma C6 cells. This study identifies CIF as a key mediator in calcium store depletion signaling to the plasma membrane.
Area of Science:
- Cellular Biology
- Neuroscience
- Biochemistry
Background:
- Capacitative calcium entry is crucial in cellular signaling.
- The mechanism transmitting intracellular calcium store depletion to plasma membrane calcium channels in rat glioma C6 cells remains unclear.
Purpose of the Study:
- To investigate the role of calcium influx factor (CIF) in mediating capacitative calcium entry in rat glioma C6 cells.
- To determine if CIF acts as the signaling molecule linking intracellular calcium store depletion to plasma membrane calcium influx.
Main Methods:
- Extraction of CIF from C6 cells treated with bombesin or thapsigargin.
- Measurement of cytoplasmic calcium concentration ([Ca2+]i) changes upon CIF addition.
- Assessment of extracellular calcium dependence and inhibition by Gd3+ and genistein.
- Evaluation of inositol 1,4,5-trisphosphate accumulation.
Main Results:
- Bombesin-treated CIF (BBS-CIF) and thapsigargin-treated CIF (TG-CIF) significantly increased [Ca2+]i in C6 cells.
- Non-treated CIF (Non-CIF) did not affect [Ca2+]i.
- The observed [Ca2+]i increase was dependent on extracellular calcium and inhibited by Gd3+ and genistein.
- BBS-CIF and TG-CIF did not alter inositol 1,4,5-trisphosphate levels.
Conclusions:
- Calcium influx factor (CIF) is identified as a mediator of capacitative calcium entry in rat glioma C6 cells.
- CIF signaling to the plasma membrane occurs independently of inositol 1,4,5-trisphosphate accumulation.
- These findings elucidate a novel mechanism for calcium signaling in glioma cells.