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Related Experiment Videos

Modulation of platelet function by extracellular adenosine triphosphate.

G Soslau1, J Parker

  • 1Department of Biological Chemistry, Hahnemann Medical School, Philadelphia, PA 19102-1192.

Blood
|August 15, 1989
PubMed
Summary

Extracellular adenosine triphosphate (ATP) affects platelet aggregation and cyclic AMP (cAMP) levels. ATP phosphorylates surface proteins, suggesting novel roles in platelet signaling and regulation beyond competitive inhibition.

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Area of Science:

  • Biochemistry
  • Hematology
  • Cell Signaling

Background:

  • Extracellular adenosine triphosphate (ATP) is known to competitively inhibit adenosine diphosphate (ADP)-induced platelet aggregation.
  • The precise physiological mechanisms of extracellular ATP's influence on platelet function remain incompletely understood.

Purpose of the Study:

  • To investigate the potential physiological roles of extracellular ATP in platelet function.
  • To explore mechanisms of ATP action beyond competitive inhibition of platelet aggregation.

Main Methods:

  • Assessing platelet aggregation in response to various agonists (collagen, epinephrine, ADP) with and without extracellular ATP.
  • Investigating ATP-induced disaggregation of maximally aggregated platelets.
  • Labeling surface-membrane proteins using extracellular gamma-32P-ATP and analyzing calcium dependency and kinetics.

Related Experiment Videos

  • Measuring intracellular cyclic AMP (cAMP) levels in platelets incubated with varying concentrations of extracellular ATP and theophylline.
  • Assessing ATP hydrolysis to adenosine using adenosine deaminase.

    • Main Results:

    • Extracellular ATP demonstrated both support for competitive inhibition and induced disaggregation of aggregated platelets, suggesting multiple mechanisms of action.
    • Extracellular ATP (7 pmol) was shown to label surface-membrane proteins in a calcium-dependent manner (1-5 mmol/L), with rapid phosphorylation kinetics.
    • Platelet cyclic AMP (cAMP) levels increased dose-dependently with extracellular ATP, showing synergistic effects with theophylline.
    • ATP was not hydrolyzed to adenosine by plasma nucleotidases.

    Conclusions:

    • Extracellular ATP modulates platelet responsiveness through mechanisms beyond competitive inhibition, including surface protein phosphorylation.
    • Phosphorylation of platelet surface proteins by extracellular ATP may regulate platelet activation and signal transduction pathways, influencing intracellular cAMP levels.
    • These findings suggest a broader physiological role for extracellular ATP in regulating platelet function and hemostasis.