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Structure and Function of Platelets01:18

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Related Experiment Video

Updated: Feb 8, 2026

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
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[Abnormal structure and dysfunction of platelets in CD226 knockout mice].

Bo Zhou1, Dongliang Zhang1, Xueqin Liu2

  • 1Department of Plastic and Reconstructive Surgery, Xijing Hospital, Air Force Military Medical University, Xi'an 710032, China.

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi = Chinese Journal of Cellular and Molecular Immunology
|July 6, 2018
PubMed
Summary
This summary is machine-generated.

The co-stimulatory molecule CD226 plays a crucial role in regulating mouse platelet function. CD226 knockout mice exhibited impaired platelet counts, prolonged bleeding times, and reduced thrombus stability.

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Area of Science:

  • Immunology
  • Hematology
  • Molecular Biology

Background:

  • Platelets are critical for hemostasis and thrombosis.
  • Co-stimulatory molecules modulate immune cell function, but their role in platelet biology is less understood.
  • CD226 is a co-stimulatory molecule expressed on immune cells.

Purpose of the Study:

  • To investigate the regulatory effect of the co-stimulatory molecule CD226 on platelet function in mice.
  • To identify proteins that interact with CD226 in platelets.

Main Methods:

  • Comparison of CD226 knockout (CD226KO) mice with wild-type (WT) C57BL/6 mice.
  • Assessment of platelet counts, bleeding times, and platelet ultrastructure (transmission electron microscopy).
  • Induction of carotid artery thrombosis using ferric chloride and evaluation of thrombus formation and stability.
  • Immunoprecipitation and mass spectrometry to identify CD226-interacting proteins in human platelets.

Main Results:

  • CD226KO mice showed significantly lower platelet counts and longer bleeding times compared to WT mice.
  • Platelet ultrastructure analysis revealed shrinkage and distortion of the endoplasmic reticulum in CD226KO mice.
  • Ferric chloride-induced thrombosis was significantly delayed, and thrombus stability was reduced in CD226KO mice.
  • Mass spectrometry identified BDNF, FABP5, and ApoA1 as potential CD226-interacting proteins in human platelets.

Conclusions:

  • The knockout of the CD226 gene significantly impairs platelet function in mice.
  • CD226 is involved in the biological activity of platelets, influencing their count, hemostatic capacity, and thrombotic potential.
  • CD226 interacts with proteins such as BDNF, FABP5, and ApoA1, suggesting novel pathways in platelet regulation.