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Transient calcium elevation in polymorphonuclear leukocytes triggered by thrombin-activated platelets

A Takahashi1, K Yamamoto, M Okuma

  • 1Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

Insights

Thrombin-activated platelets release adenosine triphosphate (ATP) and other factors that transiently increase intracellular calcium in human polymorphonuclear leukocytes (PMNs). This calcium signaling is crucial for PMN function.

Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Platelets play a critical role in hemostasis and immune responses.
  • Polymorphonuclear leukocytes (PMNs) are key immune cells involved in inflammation and host defense.
  • Calcium signaling is fundamental to cellular activation and function in both platelets and PMNs.

Purpose of the Study:

  • To investigate the effect of thrombin-activated platelets and their secreted products on intracellular calcium levels in human PMNs.
  • To identify the specific factors released by activated platelets that modulate PMN calcium concentration.

Main Methods:

  • Human PMNs were loaded with the calcium indicator fura-2.
  • The intracellular free calcium concentration ([Ca2+]i) was measured using fluorescence.
  • Supernatants from thrombin-activated platelets were applied to PMNs.
  • The effects of hexokinase and trypsin pretreatment on PMN [Ca2+]i responses were assessed.

Main Results:

  • Thrombin-activated platelets and their supernatant caused a transient increase in PMN [Ca2+]i.
  • Hexokinase pretreatment reduced the [Ca2+]i elevation, while it abrogated the response to adenosine triphosphate (ATP).
  • Trypsin pretreatment decreased the magnitude of the [Ca2+]i elevation, but did not affect the ATP-induced response.

Conclusions:

  • Thrombin-activated platelets release ATP, which contributes to the transient elevation of [Ca2+]i in PMNs.
  • Activated platelets also release a trypsin-sensitive factor that influences PMN intracellular calcium.
  • These findings elucidate a mechanism of platelet-leukocyte communication involving calcium signaling.

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