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Fibrinogen controls human platelet fibronectin internalization and cell-surface retention
1The Center Laboratory, and Department of Hematology of Anhui Provincial Hospital, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China. zhi_min@mail.hf.ah.cn
Journal of Thrombosis and Haemostasis : JTH
|June 29, 2007
Summary
Fibrinogen prevents platelet fibronectin (Fn) internalization and controls its surface retention through fibrin formation. This interaction is key for platelet aggregation.
Area of Science:
- Hematology
- Platelet Biology
- Hemostasis
Background:
- Platelet aggregation was observed in fibrinogen-deficient mice, with increased platelet fibronectin (Fn).
- This suggests a potential role for Fn in platelet aggregation independent of fibrinogen.
Observation:
- A hypofibrinogenemic patient showed significantly increased platelet Fn content.
- However, cell-surface Fn expression was markedly reduced after thrombin treatment.
- Fibrin was detected on healthy donor platelets but was negligible on the patient's platelets.
Findings:
- Fibrinogen competitively inhibits platelet Fn internalization.
- Fibrin formation on the platelet surface is crucial for retaining Fn.
- Platelet Fn is primarily released extracellularly in hypofibrinogenemia.
Implications:
- Fibrinogen regulates platelet Fn localization and interaction.
- The interplay between Fn and fibrin is a potential mechanism for promoting platelet aggregation.
- This highlights a novel pathway in hemostasis and thrombosis.
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