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Related Experiment Videos

Intracellular alkalinization augments capacitative Ca2+ entry in platelets.

Mikio Marumo1, Ichiro Wakabayashi

  • 1Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Iida-Nishi 2-2-2,Yamagata 990-9585, Japan.

Thrombosis and Haemostasis
|December 4, 2003
PubMed
Summary

Intracellular alkalinization enhances platelet calcium signaling and aggregation. This finding suggests that increasing intracellular pH is a key factor in regulating platelet function and calcium entry.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Platelet signal transduction is crucial for hemostasis and thrombosis.
  • Capacitative calcium entry (CCE) plays a vital role in platelet activation.
  • The influence of intracellular pH on CCE in platelets requires further elucidation.

Purpose of the Study:

  • To investigate the role of intracellular alkalinization in regulating capacitative calcium entry (CCE) in platelets.
  • To determine if elevated intracellular pH enhances CCE and subsequent platelet aggregation.

Main Methods:

  • Platelet intracellular pH was manipulated using ammonium chloride (NH4Cl) for alkalinization and propionate for acidification.
  • CCE was induced by extracellular calcium addition after depleting intracellular stores with thapsigargin.

Related Experiment Videos

  • Platelet aggregation was measured following CCE induction.
  • The effects of NH4Cl, propionate, and SKF-96365 (a CCE inhibitor) on CCE and aggregation were assessed.
  • Extracellular alkalosis was induced using Tris buffer.

    • Main Results:

    • NH4Cl-induced intracellular alkalinization significantly augmented CCE and platelet aggregation.
    • This augmentation was abolished by the CCE inhibitor SKF-96365 and by propionate-induced intracellular acidification.
    • Extracellular alkalosis also augmented CCE and aggregation, with partial inhibition by propionate.
    • These results indicate that intracellular alkalinization partially mediates the effects of extracellular alkalosis on CCE.

    Conclusions:

    • Intracellular alkalinization is a significant signaling mechanism that potentiates capacitative calcium entry in platelets.
    • Modulating intracellular pH represents a potential therapeutic target for conditions involving platelet hyperreactivity.