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. 2015 Oct 30;29(6):437-444.
doi: 10.7555/JBR.29.20150121. Online ahead of print.

Platelets in hemostasis and thrombosis: Novel mechanisms of fibrinogen-independent platelet aggregation and fibronectin-mediated protein wave of hemostasis

Yan Hou  1   2 , Naadiya Carrim  1   3   4 , Yiming Wang  1   3   4 , Reid C Gallant  1   3 , Alexandra Marshall  1 , Heyu Ni  1   3   5
Affiliations

Platelets in hemostasis and thrombosis: Novel mechanisms of fibrinogen-independent platelet aggregation and fibronectin-mediated protein wave of hemostasis

Yan Hou et al. J Biomed Res. .

Abstract

Platelets are small anucleate cells generated from megakaryocytes in the bone marrow. Although platelet generation, maturation, and clearance are still not fully understood, significant progress has been made in the last 1-2 decades. In blood circulation, platelets can quickly adhere and aggregate at sites of vascular injury, forming the platelet plug (i.e. the first wave of hemostasis). Activated platelets can also provide negatively charged phosphatidylserinerich membrane surface that enhances cell-based thrombin generation, which facilitates blood coagulation (i.e. the second wave of hemostasis). Platelets therefore play central roles in hemostasis. However, the same process of hemostasis may also cause thrombosis and vessel occlusion, which are the most common mechanisms leading to heart attack and stroke following ruptured atherosclerotic lesions. In this review, we will introduce the classical mechanisms and newly discovered pathways of platelets in hemostasis and thrombosis, including fibrinogen-independent platelet aggregation and thrombosis, and the plasma fibronectin-mediated "protein wave" of hemostasis that precedes the classical first wave of hemostasis. Furthermore, we briefly discuss the roles of platelets in inflammation and atherosclerosis and the potential strategies to control atherothrombosis.

Keywords: fibrinogen; fibronectin; integrin αIIbβ3; platelets; thrombosis and hemostasis.

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Conflict of interest statement

CLC number: R331.1+43 Document code: A

The authors reported no conflict of interests

Figures

Fig. 1
Fig. 1. At the site of vascular injury plasma fibronectin deposition occurs even before platelets adhere.
Platelets may release their internalized plasma fibronectin from intracellular granules. Platelet receptors then bind physiological ligands, such as VWF and collagen, activating integrin αIIbβ3 and resulting in fibrinogen binding and subsequent platelet aggregation. Thrombin is generated on the negatively charged platelet surface and further activates platelets and contributes to the coagulation cascade. In a growing hemostatic plug/thrombus, the fibrin and fibronectin matrix is usually formed at the interface between the injured vessel wall and the platelet plug.
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