Differentiation of answer of glioma C6 cells to SERCA pump inhibitors by actin disorganization

Capacitative calcium entry, usually evoked by receptor–ligand binding, may be also studied in the model system of calcium release after SERCA pump inhibition. We have previously found that disorganization of actin cytoskeleton has no effect on calcium influx into glioma C6 cells after thapsigargin a...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2004-10, Vol.323 (3), p.870-875
Main Authors: Supłat, Dorota, Targos, Berenika, Sabała, Paweł, Barańska, Jolanta, Pomorski, Paweł
Format: Article
Language:English
Subjects:
Actin cytoskeleton
Actin Cytoskeleton - metabolism
Actin Cytoskeleton - ultrastructure
Actins - metabolism
Actins - ultrastructure
Animals
Calcium - metabolism
Calcium-Transporting ATPases - antagonists & inhibitors
Calcium-Transporting ATPases - metabolism
Cell Line, Tumor
CPA
Cytochalasin D - pharmacology
DBHQ
Endoplasmic Reticulum - metabolism
Endoplasmic Reticulum - ultrastructure
Glioma - metabolism
Glioma - pathology
Glioma C6
Rats
Sarcoplasmic Reticulum Calcium-Transporting ATPases
SERCA
Store-mediated Ca2+ influx
Thapsigargin - pharmacology
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Summary:Capacitative calcium entry, usually evoked by receptor–ligand binding, may be also studied in the model system of calcium release after SERCA pump inhibition. We have previously found that disorganization of actin cytoskeleton has no effect on calcium influx into glioma C6 cells after thapsigargin administration [Biochem. Biophys. Res. Commun. 296 (2002) 484]. In the present work we show that the effect of other SERCA pump inhibitors depends on the endoplasmic reticulum distribution in a cell. Changing this distribution leads to changes in calcium release from ER stores. Intensity of calcium influx in the capacitative phase of cell answer does not depend on actin cytoskeleton state; however, administration of cytochalasin D significantly slows down signal build-up. While cyclopiazonic acid acts very similarly to thapsigargin, cytoskeleton disorganization leads to rise of calcium signal after administration of 2,5-di-(t-butyl)-1,4-benzohydroquinone. This effect may be caused by specific binding of this inhibitor to SERCA3 isoform of pump protein only.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2004.08.155