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Identification of mRNA coding for factor VII protein in human alveolar macrophages--coagulant expression may be

M P McGee1, R Wallin, R Devlin

  • 1Department of Medicine, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.

Insights

Alveolar macrophages produce factor VII mRNA, a clotting factor precursor. However, they lack the necessary enzyme activity for functional factor VII production, limiting its expression during inflammation.

Area of Science:

  • Immunology
  • Hematology
  • Molecular Biology

Background:

  • Monocytes and macrophages are implicated in initiating coagulation during inflammation.
  • Previous studies found vitamin K-dependent coagulation factors associated with monocytes/macrophages.
  • No prior reports identified mRNA for vitamin K-dependent proteins in these cells.

Purpose of the Study:

  • To investigate the synthesis of factor VII mRNA in human alveolar macrophages.
  • To determine the presence of vitamin K-dependent carboxylase activity in these cells.
  • To assess the functional expression of coagulation factor VII in alveolar macrophages.

Main Methods:

  • Hybridization with a complementary DNA probe to detect factor VII mRNA in RNA from isolated human alveolar macrophages.
  • Assays for vitamin K-dependent carboxylase activity in macrophages before and after culture.
  • Kinetic assays to measure factor VII activity during macrophage culture.

Main Results:

  • Factor VII mRNA was detected in freshly isolated human alveolar macrophages.
  • Vitamin K-dependent carboxylase activity was not detectable in macrophages, unlike control hepatoma cells.
  • No increase in factor VII activity was observed during macrophage culture, despite increased tissue factor activity.

Conclusions:

  • Human alveolar macrophages synthesize factor VII mRNA in vivo.
  • The absence of gamma-carboxylase activity prevents the post-translational modification of factor VII.
  • Functional expression of coagulation factor VII in alveolar macrophages is likely limited by a deficiency in post-ribosomal processing.

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