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Platelet-derived microvesicles induce intracellular calcium mobilization in human platelets

Pooja Yadav1, Abhishek R Panigrahi1, Samir K Beura1

  • 1Department of Zoology, School of Biological Sciences, Central University of Punjab, Bathinda, India.

Cell Biology International
|August 31, 2023
PubMed

Insights

Platelet-derived microvesicles (PMVs) elevate platelet calcium levels through intracellular and extracellular pathways. This research clarifies PMV impact on calcium signaling in human platelets.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Hematology

Background:

  • Platelet-derived microvesicles (PMVs) are abundant in circulation and implicated in various diseases.
  • PMVs contain cargo that can modulate target cell functions, particularly calcium signaling.
  • Calcium ions are crucial for cellular processes, including hemostasis and thrombosis.

Purpose of the Study:

  • To investigate the effect of PMVs on calcium mobilization in human platelets.
  • To elucidate the mechanisms underlying PMV-induced calcium changes in platelets.

Main Methods:

  • Quantification of intracellular calcium levels in platelets upon PMV exposure.
  • Assessment of calcium release from intracellular stores (dense tubular system, mitochondria).
  • Evaluation of extracellular calcium influx, including store-operated calcium entry (SOCE).

Main Results:

  • PMVs significantly increase platelet intracellular calcium in a dose-dependent manner.
  • PMV-mediated calcium release involves intracellular stores and extracellular calcium influx via SOCE.
  • The sarcoendoplasmic reticulum calcium ATPase (SERCA) is not involved in PMV-induced calcium elevation.

Conclusions:

  • PMVs play a critical role in modulating platelet calcium homeostasis.
  • Understanding PMV-calcium interactions offers insights into platelet activation and thrombosis.
  • These findings contribute to comprehending cell behavior in PMV-rich conditions.
Keywords:
PLC-IP3intracellular calciummicrovesiclesplateletsstore-operated calcium entry

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