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Calcium signaling in human platelets.

T J Rink1, S O Sage

  • 1Smith Kline & French Research Limited, Welwyn, Herts, United Kingdom.

Annual Review of Physiology
|January 1, 1990
PubMed
Summary

Recent advances reveal complex calcium (Ca2+) mobilization in platelets, with Ins1,4,5-trisphosphate likely mediating internal release. Multiple pathways for Ca2+ entry are identified, including ADP receptor-linked and store-operated mechanisms.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Hematology

Background:

  • Platelet calcium (Ca2+) mobilization is crucial for hemostasis and thrombosis.
  • Recent years have seen significant progress in understanding Ca2+ signaling in platelets.

Purpose of the Study:

  • To review and synthesize recent advances in platelet Ca2+ mobilization.
  • To elucidate the mechanisms of internal Ca2+ release and external Ca2+ entry in platelets.

Main Methods:

  • Stopped-flow fluorescence spectroscopy to analyze receptor-mediated Ca2+ entry.
  • Patch-clamp electrophysiology applied to platelets.
  • Review of existing literature on platelet Ca2+ signaling.

Main Results:

  • Evidence supports a role for Ins1,4,5-trisphosphate in internal Ca2+ release, though kinetics require further study.
  • At least three distinct pathways for Ca2+ entry exist, including ADP receptor-coupled, second messenger-mediated, and store-operated entry.
  • Patch-clamp studies identified voltage-gated K+ channels and ADP-stimulated channels potentially involved in Ca2+ elevation.

Conclusions:

  • Platelet Ca2+ mobilization involves intricate mechanisms for both release and entry.
  • While Ins1,4,5-trisphosphate is implicated, alternative pathways for internal Ca2+ release may exist.
  • Further research is needed to fully characterize the identified Ca2+ entry pathways and regulatory mechanisms.

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