ArticlePflugers Archiv : European journal of physiology1995
Cholecystokinin-stimulated enzyme secretion from dispersed rabbit pancreatic acinar cells: phosphorylation-dependent changes in potency and efficacy.
Article in Pflugers Archiv : European journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors at 1 institution in 1 country.
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Abstract
In order to establish a regulatory role for phosphoproteins in receptor-stimulated enzyme secretion, dispersed rabbit pancreatic acinar cells were stimulated with the COOH-terminal octapeptide of cholecystokinin (CCK8) in the absence and presence of staurosporine and/or 12-O-tetradecanoylphorbol 13-acetate (TPA) or forskolin. The dose/response curve for the stimulatory effect of CCK8 on amylase secretion was biphasic, with a mean half-maximal concentration (EC50) of 21 pM. Staurosporine (1 microM) did not affect secretion elicited by CCK8 concentrations below 0.1 nM, but reduced the response to CCK8 concentrations above 0.1 nM. As a result, the mean EC50 for CCK8 decreased to 8 pM and its efficacy to 70%. The phorbol ester TPA (0.1 microM) attenuated secretion evoked by CCK8 concentrations below 0.1 nM and potentiated the response to CCK8 concentrations above 0.1 nM. As a result, the mean EC50 for CCK8 increased to 0.14 nM and its efficacy to 300%. Staurosporine abolished both the inhibitory and the potentiating effect of TPA, thereby turning the inhibitory effect into a strong potentiating effect. As a result, the mean EC50 for CCK8 decreased to 3 pM, whereas its efficacy increased to 190%. Forskolin (30 microM) potentiated the response to both the lower and the higher CCK8 concentrations. As a result, the mean EC50 for CCK8 increased to 28 pM and its efficacy to 300%. Staurosporine enhanced the potentiating effect of forskolin at CCK8 concentrations below 0.1 nM, but abolished potentiation at CCK8 concentrations above 0.1 nM. As a result, the mean EC50 for CCK8 decreased to 1.4 pM, whereas its efficacy increased to 260%. The data presented demonstrate that the apparent sensitivity of dispersed pancreatic acinar cells to stimulation of the process of enzyme secretion by CCK8 decreases when kinases are activated and increases when kinases are inactivated. Moreover, they show that the efficacy of CCK8 increases by the action of kinases, both sensitive and insensitive to staurosporine.
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