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Volume 272, Number 50, Issue of December 12, 1997 pp. 31435-31440
(Received for publication, April 28, 1997, and in revised form, September 29, 1997)
From the Department of Veterans Affairs Medical Center, The regulation of cytosolic
Ca2+ is important for a variety of cell functions.
One non-inositol 1,4,5-trisphosphate (IP3) compound that
may regulate Ca2+ is palmitoyl-coenzyme A (CoA), a fatty
acid-CoA that is reported to cause Ca2+ release from
intracellular stores of oocytes, myocytes, and hepatocytes. To study the role of palmitoyl-CoA in the pancreatic acinar cell, rat
pancreatic acini were isolated by collagenase digestion, permeablized with streptolysin O, and the release of Ca2+ from internal
stores was measured with fura-2. Palmitoyl-CoA released
Ca2+ from internal stores (EC50 = 14 µM). The palmitoyl-CoA-sensitive pool was distinct from,
and overlapping with the IP3-sensitive Ca2+
pool. The effects of submaximal doses of IP3 or cyclic
ADP-ribose plus palmitoyl-CoA were additive. Fatty acid-CoA derivatives
with carbon chain lengths of 16-18 were the most potent and
efficacious. Ryanodine and caffeine or elevated resting
[Ca2+] sensitized the Ca2+ pool to the
actions of palmitoyl-CoA. Fatty acid-CoA levels in pancreatic acini
were measured by extraction with 2-propanol/acetonitrile, followed by
separation and quantification using reverse phase high performance
liquid chromatography, and were found to be 10.17 ± 0.93 nmol/mg
protein. These data suggest the presence of an IP3-insensitive palmitoyl-CoA-sensitive Ca2+
store in pancreatic acinar cells and suggest that palmitoyl-CoA may be
needed for Ca2+-induced Ca2+ release.
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