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Related Experiment Videos

Multiple signaling pathways control stimulus-secretion coupling in rat peritoneal mast cells.

R Penner1

  • 1Max-Planck-Institut für Biophysikalische Chemie, Göttingen, Federal Republic of Germany.

Proceedings of the National Academy of Sciences of the United States of America
|December 1, 1988
PubMed
Summary

Mast cells use a G protein signaling pathway distinct from inositolphospholipid turnover to trigger secretion. This pathway, alongside calcium signaling and protein kinase C, regulates mast cell degranulation.

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Area of Science:

  • Cellular Biology
  • Immunology
  • Biochemistry

Background:

  • Mast cells are key immune cells involved in allergic responses.
  • Stimulus-secretion coupling in mast cells is complex and involves various signaling pathways.

Purpose of the Study:

  • To investigate the roles of intracellular calcium ([Ca2+]i) and signaling pathways in rat peritoneal mast cell secretion.
  • To elucidate the involvement of G protein-mediated signaling and inositolphospholipid breakdown in mast cell degranulation.

Main Methods:

  • Fura-2 fluorescence measurements to assess intracellular calcium ([Ca2+]i).
  • Membrane capacitance measurements to quantify secretory responses.
  • Stimulation with secretagogues like Compound 48/80 and GTP[gamma-S].
  • Inhibition studies using guanosine 5'-[beta-thio]diphosphate, neomycin, pertussis toxin, cAMP, and phorbol 12-myristate 13-acetate (PMA).

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Main Results:

  • Compound 48/80 and GTP[gamma-S] induced transient [Ca2+]i rises and secretion.
  • Inositolphospholipid breakdown mediated by G protein was implicated in stimulus-secretion coupling.
  • Pertussis toxin affected secretion but not Ca2+ transients, suggesting a pertussis toxin-insensitive pathway.
  • cAMP inhibited secretion but not Ca2+ transients, while PMA reduced Ca2+ requirement for secretion and abolished Ca2+ transients.

Conclusions:

  • Mast cell secretion is regulated by a G protein-involved pathway distinct from inositolphospholipid turnover.
  • Inositolphospholipid pathway increases [Ca2+]i and enhances secretion sensitivity via protein kinase C.
  • PMA exerts negative feedback on the inositolphospholipid pathway, and cAMP may inhibit the unidentified signaling pathway.