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Driss Zoukhri, Robin R. Hodges, Christian Sergheraert, Darlene A. Dartt; Cholinergic-Induced Ca2+ Elevation in Rat Lacrimal Gland Acini Is Negatively Modulated by PKCδ and PKCε. Invest. Ophthalmol. Vis. Sci. 2000;41(2):386-392.
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purpose. To investigate the role of protein kinase C (PKC) in cholinergic
agonist-induced Ca2+ elevation in lacrimal gland acini.
methods. Lacrimal gland acini were prepared by collagenase digestion, and
changes in intracellular Ca2+ ([Ca2+]i) were measured using fura-2 as a
results. Preactivation of PKC by phorbol 12-myristate 13-acetate (PMA), or
inhibition of protein phosphatase type 1/2A (PP1/2A) by calyculin A,
decreased both the [Ca2+]i transient and the
plateau of [Ca2+]i induced by increasing
concentrations of carbachol, a cholinergic agonist. Staurosporine, an
inhibitor of PKC, completely reversed the effect of PMA. Inhibition of
the Ca2+-independent PKC isoforms PKCδ and -ε, but not
the Ca2+-dependent isoform PKCα substantially reversed
the inhibitory effect of PMA on cholinergic agonist-induced
Ca2+ elevation. The inhibitory effect of PMA was obtained
only in the presence of extracellular Ca2+, suggesting that
PKC inhibits the influx of Ca2+. PMA completely inhibited
the cholinergic agonist-induced plateau of[
Ca2+]i. PMA and calyculin A decreased both
the [Ca2+]i transient and the plateau of[
Ca2+]i induced by thapsigargin, further
supporting the idea that PKC modulates the entry of Ca2+.
conclusions. In the lacrimal gland, agonist-induced changes in[
Ca2+]i are negatively regulated by
PKC-dependent phosphorylation of a target protein(s) that is sensitive
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