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Updated: Aug 6, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Endocytosis of plasma-derived factor V by megakaryocytes occurs via a clathrin-dependent, specific membrane binding

B A Bouchard1, J L Williams, N T Meisler

  • 1Department of Biochemistry, University of Vermont College of Medicine, Burlington, VT 05405, USA.

Journal of Thrombosis and Haemostasis : JTH
|March 8, 2005
PubMed

Insights

Megakaryocytes, the cells that produce platelets, actively endocytose (internalize) factor V through a specific mechanism. This process is distinct from how platelets handle factor V and involves clathrin-dependent pathways.

Area of Science:

  • Hematology
  • Cell Biology
  • Molecular Biology

Background:

  • Megakaryocytes are crucial for platelet production and play roles in hemostasis.
  • Understanding protein uptake mechanisms in megakaryocytes is vital for comprehending their function.
  • Factor V is essential for blood coagulation, but its cellular uptake by megakaryocytes is not well understood.

Purpose of the Study:

  • To investigate the cellular mechanisms by which megakaryocytes endocytose factor V.
  • To determine if factor V endocytosis is specific and regulated in megakaryocytes.
  • To compare factor V endocytosis with that of other proteins like fibrinogen and factor IX.

Main Methods:

  • Analysis of factor V endocytosis in megakaryocytes derived from CD34(+) cells and megakaryocyte-like cell lines (MEG-01, CMK).
  • Comparison of endocytosis in differentiated versus undifferentiated cell lines and with platelets.
  • Investigation using fibrinogen and factor IX as control proteins.
  • Assessment of specificity using cell lines with differential protein uptake (CHRF-288) and in the presence of other plasma proteins.
  • Examination of the endocytic pathway, including clathrin dependence.

Main Results:

  • Megakaryocytes, but not platelets, efficiently endocytosed factor V.
  • Differentiated megakaryocyte cell lines showed significantly increased factor V and fibrinogen endocytosis.
  • Factor IX was not endocytosed by any cell type examined.
  • Factor V endocytosis was shown to be specific, independent of other plasma proteins, and clathrin-dependent, suggesting a receptor-mediated mechanism.

Conclusions:

  • Megakaryocytes possess a specific and independent mechanism for endocytosing factor V.
  • This endocytic process is likely receptor-mediated and clathrin-dependent.
  • The findings elucidate a novel cellular mechanism for factor V regulation within megakaryocytes.

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