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Related Experiment Videos

Stimulus-secretion coupling in pancreatic acinar cells.

D B Burnham, J A Williams

    Journal of Pediatric Gastroenterology and Nutrition
    |January 1, 1984
    PubMed
    Summary

    Secretagogues like CCK and acetylcholine elevate calcium (Ca2+) in pancreatic cells, while VIP and secretin increase cyclic AMP. Both pathways activate enzyme secretion, with cyclic AMP potentially acting independently of Ca2+ in some cases.

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    Area of Science:

    • Cell biology
    • Molecular signaling
    • Gastroenterology

    Background:

    • Pancreatic acinar cells secrete enzymes crucial for digestion.
    • Secretagogues trigger enzyme secretion through complex signaling pathways.
    • The roles of calcium (Ca2+) and cyclic AMP in this process are key areas of investigation.

    Purpose of the Study:

    • To elucidate the mechanisms by which Ca2+ and cyclic AMP activate enzyme secretion in pancreatic acinar cells.
    • To investigate the role of receptor binding in intracellular Ca2+ mobilization.
    • To explore the involvement of membrane phosphatidylinositol metabolism in Ca2+ signaling.

    Main Methods:

    • Summarizing signaling pathways for Ca2+ and cyclic AMP secretagogues.
    • Analyzing receptor-mediated Ca2+ elevation.

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  • Examining potential diffusable mediators in Ca2+ mobilization.
  • Investigating the role of membrane phosphatidylinositol metabolism.

    • Main Results:

    • CCK and acetylcholine binding elevates cytoplasmic Ca2+ via incompletely understood mechanisms.
    • VIP and secretin binding leads to cyclic AMP accumulation.
    • Cyclic AMP potentiates Ca2+-mediated secretion and may act independently in some species.
    • Kinases (Protein Kinase A, C) and phosphatases are activated by these second messengers, altering protein phosphorylation.

    Conclusions:

    • Enzyme secretion in pancreatic acinar cells is regulated by both Ca2+ and cyclic AMP signaling pathways.
    • The interplay between these pathways, particularly at the level of kinases and phosphatases, is critical for potentiation of secretion.
    • Further research is needed to fully understand the mechanisms of Ca2+ mobilization and the role of phosphatidylinositol metabolism.