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Delineating Zinc Influx Mechanisms during Platelet Activation.

Sahithi J Kuravi1, Niaz S Ahmed1, Kirk A Taylor2

  • 1School of Life Sciences, Anglia Ruskin University, Cambridge CB1 1PT, UK.

International Journal of Molecular Sciences
|July 29, 2023
PubMed
Summary

Platelets release zinc (Zn2+) which activates them by entering the cell. This zinc influx occurs through TRP channels and the NCX exchanger, a process termed store-operated zinc entry (SOZE).

Keywords:
NCXTRP channelsZIP7aggregationcation signalingplateletsstore-operated calcium entrystore-operated zinc entryzinczinc entryzinc-induced platelet activation

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Area of Science:

  • Hematology
  • Cellular Physiology
  • Biochemistry

Background:

  • Platelets release zinc (Zn2+) during hemostasis.
  • Extracellular zinc ([Zn2+]o) activates platelets via influx into the cytosol.
  • Mechanisms of Zn2+ influx into platelets were previously unknown.

Purpose of the Study:

  • To elucidate the mechanisms of extracellular zinc ([Zn2+]o) influx into platelets.
  • To investigate the role of zinc influx in platelet activation and signaling.
  • To identify the specific channels and pathways involved in zinc entry.

Main Methods:

  • Measured intracellular zinc ([Zn2+]i) using fluozin-3, fluorometry, and flow cytometry.
  • Assessed platelet activation via light transmission aggregometry.
  • Detected phosphoproteins using Western blotting.
  • Investigated the role of TRP channels, NCX, ZIP7, Orai1, and IP3R.

Main Results:

  • [Zn2+]o influx and platelet activation were blocked by inhibiting the sodium/calcium exchanger (NCX), TRP channels, and ZIP7.
  • Cation store depletion regulated Zn2+ influx, indicating a store-operated pathway (SOZE).
  • [Zn2+]o stimulation led to phosphorylation of PKC substates, MLC, and β3 integrin.
  • Platelet activation induced ZIP7 phosphorylation and subsequent Zn2+ influx via Orai1, ZIP7, or IP3R pathways.

Conclusions:

  • Platelets detect and respond to extracellular zinc ([Zn2+]o) through influx via TRP channels and the NCX exchanger.
  • Platelet activation involves ZIP7 externalization, regulating further zinc influx.
  • Increased intracellular zinc ([Zn2+]i) activates cation-dependent enzymes, impacting thrombosis and hemostasis.