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Cholinergic-Induced Ca²⁺ Elevation in Rat Lacrimal Gland Acini Is Negatively Modulated by PKC and PKC

From ¹ Schepens Eye Research Institute and the Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; and ² Institut Pasteur de Lille, Centre National de la Recherche Scientifique, Lille, France.

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 fluorescent probe.

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 PKC and -, but not the Ca²⁺-dependent isoform PKC 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 to PP1/2A.

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