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Diabetes 52:1723-1731, 2003
© 2003 by the American Diabetes Association, Inc.

Dynamics of Calcium Clearance in Mouse Pancreatic ß-Cells

Liangyi Chen1, Duk-Su Koh1,2, and Bertil Hille1

1 Department of Physiology & Biophysics, School of Medicine, University of Washington, Seattle, Washington
2 Department of Physics, Pohang University of Science & Technology, Pohang, Korea

Pancreatic ß-cells maintain glucose homeostasis by their regulated Ca2+-dependent secretion of insulin. Several cellular mechanisms control intracellular Ca2+ levels, but their relative significance in mouse ß-cells is not fully known. We used photometry to measure the dynamics of cytosolic Ca2+ ([Ca2+]i) clearance after brief, depolarization-induced Ca2+ entry. Treatment with thapsigargin or cyclopiazonic acid, inhibitors of the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) pumps, nearly doubled the peak and slowed the decay of the depolarization-induced Ca2+ transients. The remaining thapsigargin-insensitive decay was slowed further by inhibition of the plasma membrane Ca2+-ATPase (PMCA) and plasma membrane Na+/Ca2+ exchanger (NCX) via alkalization of the bath solution, by adding lanthanum, or by substitution of Na+ with Li+. Mitochondrial Ca2+ uptake contributed little to clearance in thapsigargin-pretreated cells. Together, the SERCA, PMCA, and NCX transport mechanisms accounted for 89 to 97% of clearance in normal solutions. We developed a quantitative model for the dynamic role of removal mechanisms over a wide range of [Ca2+]i. According to our model, 50 to 64% of initial Ca2+ removal is via the SERCA pump, whereas the NCX contributes 21–30% of the extrusion at high [Ca2+]i, and the PMCA contributes 21–27% at low [Ca2+]i.

Address correspondence and reprint requests to Bertil Hille, Department of Physiology & Biophysics, School of Medicine, University of Washington, Box 357290, Seattle, WA 98195-7290. E-mail: lychen{at}u.washington.edu


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