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Updated: Aug 9, 2026
Use of a Monocyte Monolayer Assay to Evaluate Fcγ Receptor-mediated Phagocytosis
Published on: January 2, 2017
Human monocytes have prothrombin cleaving activity
Abstract:
A proportion of human monocytes form long needles of fibrin on their surfaces when they are briefly exposed to human plasma. A number of coagulation factor deficient plasmas (II, V, VII, VIII, von Willebrand, IX, X, XI and XII) were tested for their ability to promote formation of this fibrin. Monocytes failed to make fibrin only in Factor II or prothrombin deficient plasma. Thrombin is involved in the manufacture of monocyte fibrin as shown by the ability of the thrombin specific inhibitor, hirudin, to block the process and by the demonstration that monocytes are able to cleave prothrombin to thrombin, an activity which increases with time of monocyte incubation at 37 degrees C. These results indicate that human monocytes possess a prothrombin cleaving activity although it remains unclear how this activity is generated. It is speculated that thrombin serves a necessary role in both wound healing and tissue repair.
Insights
Human monocytes generate fibrin on their surfaces using thrombin (a clotting protein). This process requires factor II (prothrombin) and suggests monocytes have a prothrombin-cleaving ability crucial for tissue repair.
Area of Science:
- Hematology
- Cell Biology
- Biochemistry
Background:
- Human monocytes can form fibrin on their surfaces upon plasma exposure.
- The specific coagulation factors involved in this monocyte-derived fibrin formation are not fully elucidated.
Purpose of the Study:
- To investigate the role of coagulation factors in monocyte-induced fibrin formation.
- To determine if monocytes possess intrinsic procoagulant activity.
Main Methods:
- Testing monocyte fibrin formation in various factor-deficient plasmas.
- Utilizing a thrombin-specific inhibitor (hirudin) to assess thrombin's role.
- Measuring monocyte prothrombin cleavage over time.
Main Results:
- Monocyte fibrin formation was impaired only in factor II (prothrombin) deficient plasma.
- Hirudin inhibited fibrin formation, confirming thrombin's necessity.
- Monocytes demonstrated an increasing ability to cleave prothrombin to thrombin with incubation time.
Conclusions:
- Human monocytes possess a prothrombin-cleaving activity, generating thrombin necessary for fibrin formation.
- Thrombin likely plays a significant role in monocyte-mediated wound healing and tissue repair processes.
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