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Ca(2+)-induced Ca2+ release in insulin-secreting cells
M S Islam1, P Rorsman, P O Berggren
1Rolf Luft Center for Diabetes Research, Department of Endocrinology, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
FEBS Letters
|January 27, 1992
Summary
Thimerosal releases calcium from intracellular stores in insulin-secreting cells, independent of inositol trisphosphate signaling. This calcium release mechanism may involve calcium-induced calcium release in these cells.
Area of Science:
- Cellular biology
- Endocrinology
- Pharmacology
Background:
- Insulin secretion is regulated by intracellular calcium (Ca2+) levels.
- Understanding calcium pools and release mechanisms is crucial for studying pancreatic beta-cell function.
Purpose of the Study:
- To investigate the effect of the sulphydryl reagent thimerosal on intracellular Ca2+ release in insulin-secreting cells.
- To characterize the specific intracellular Ca2+ pool affected by thimerosal.
Main Methods:
- Using permeabilized RINm5F insulin-secreting cells.
- Dose-dependent application of thimerosal.
- Assessing Ca2+ release and its sensitivity to Ins(1,4,5)P3 and thapsigargin.
- Investigating the effect of dithiothreitol and caffeine.
Main Results:
- Thimerosal (50 microM) induced a dose-dependent Ca2+ release from a non-mitochondrial intracellular pool.
- This Ca2+ release was insensitive to inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) and thapsigargin.
- Thimerosal did not affect the Ins(1,4,5)P3-sensitive Ca2+ pool.
- The release was reversible by dithiothreitol and potentiated by caffeine.
Conclusions:
- Thimerosal releases Ca2+ from an Ins(1,4,5)P3-insensitive intracellular pool in RINm5F cells.
- These findings suggest the presence of a calcium-induced calcium release mechanism in insulin-secreting cells.