Platelets: Physiology and biochemistry

Department of Anaesthesiology and Intensive Care, Experimental and Clinical Haemostasis, University-Hospital Münster, Münster, Germany.
Seminars in Thrombosis and Hemostasis (Impact Factor: 3.69). 02/2005; 31(4):381-92. DOI: 10.1055/s-2005-916671
Source: PubMed

ABSTRACT Platelets are specialized blood cells that play central roles in physiologic and pathologic processes of hemostasis, inflammation, tumor metastasis, wound healing, and host defense. Activation of platelets is crucial for platelet function that includes a complex interplay of adhesion and signaling molecules. This article gives an overview of the activation processes involved in primary and secondary hemostasis, for example, platelet adhesion, platelet secretion, platelet aggregation, microvesicle formation, and clot retraction/stabilization. In addition, activated platelets are predominantly involved in cross talk to other blood and vascular cells. Stimulated "sticky" platelets enable recruitment of leukocytes at sites of vascular injury under high shear conditions. Platelet-derived microparticles as well as soluble adhesion molecules, sP-selectin and sCD40L, shed from the surface of activated platelets, are capable of activating, in turn, leukocytes and endothelial cells. This article focuses further on the new view of receptor-mediated thrombin generation of human platelets, necessary for the formation of a stable platelet-fibrin clot during secondary hemostasis. Finally, special emphasis is placed on important stimulatory and inhibitory signaling pathways that modulate platelet function.

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    • "The addition of 10% collagen to the xenogenic BSM enhanced platelet degranulation in a obvious manner. Platelet consumption also stands for degranulation and cytokine release (Jurk & Kehrel 2005). In accordance, cytokine concentrations analog to the respective platelet activation were expected. "
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    ABSTRACT: INTRODUCTION: Initial platelet activation with subsequent cytokine release at the defect site plays a crucial role in tissue integration. The aim of this study was to evaluate the influence of topographic and biomimetic collagen modifications of a xenogenic bone substitute material (BSM) on in vitro platelet activation and cytokine release. MATERIAL AND METHODS: Three types of xenogenic BSM were used. Two BSM with different levels of granularity (large granule BSM [XBSM/L], small granule BSM [XBSM/S]) and a BSM with collagen (XBSM/C). All three samples were incubated with platelet concentrate of four healthy volunteers at room temperature for 15 min. For all groups, highly thrombogenic collagen type 1 served as a reference and an additional preparation with platelet concentrate only (without XBSM) served as control. Platelet count and cytokine release of VEGF, PDGF, TGF-β, and IGF into the supernatant were measured. RESULTS: Compared with the control group, XBSM/C showed an increase in platelets consumption (mean 41,000 ± 26,000/ml vs. 471,000 ± 38,000/ml), cytokine release of VEGF (mean 46.8 ± 7.2 pg/ml vs. 18.8 ± 2.7 pg/ml), and PDGF (mean 18,350 ± 795 pg/ml vs. 2726 ± 410 pg/ml) but not IGF (194,728 ± 51,608 pg/ml vs. 1,333,911 ± 35,314 pg/ml). There was also an increase in cytokine release of TGF-ß in XBSM/C compared with XBSM/S (77,188 ± 27,413 pg/ml vs. 38,648 ± 13,191 pg/ml), but no such difference when compared with XBSM/L (77,188 ± 27,413 pg/ml vs. 53,309 ± 29,430 pg/ml). XBSM/L showed higher platelets consumption (301,000 ± 45,000 vs. 415,000 ± 98,000) and a higher cytokine release of PDGF (3511 ± 247 pg/ml vs. 3165 ± 78 pg/ml) compared with XBSM/S. There was no distinct difference in the levels of VEGF, TGF-ß, and IGF between XBSM/L and XBSM/S. CONCLUSIONS: Topographic as well as biomimetic modifications of the xenogenic BSM showed an increased platelet activation and cytokine release in vitro. This effect on the intrinsic healing cascade could result in comparable enhanced soft- and hard-tissue regeneration in vivo.
    Clinical Oral Implants Research 03/2013; 25(7). DOI:10.1111/clr.12153 · 3.12 Impact Factor
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    • "The platelet lifespan is approximately 7 to 9 days, which they spend circulating in the blood in their resting form. When adhered to exposed endothelium or activated by agonists, they change their shape and secrete the contents of the granules (including ADP, fibrinogen, and serotonin), which is followed by platelet aggregation [7]. Initiation of the signaling event within the platelet leads to the reorganization of the platelet cytoskeleton, which is visible as an extremely rapid shape change [17] "
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    ABSTRACT: Platelet-derived Growth Factors (GFs) are biologically active peptides that enhance tissue repair mechanisms such as angiogenesis, extracellular matrix remodeling, and cellular effects as stem cells recruitment, chemotaxis, cell proliferation, and differentiation. Platelet-rich plasma (PRP) is used in a variety of clinical applications, based on the premise that higher GF content should promote better healing. Platelet derivatives represent a promising therapeutic modality, offering opportunities for treatment of wounds, ulcers, soft-tissue injuries, and various other applications in cell therapy. PRP can be combined with cell-based therapies such as adipose-derived stem cells, regenerative cell therapy, and transfer factors therapy. This paper describes the biological background of the platelet-derived substances and their potential use in regenerative medicine.
    International Journal of Peptides 02/2012; 2012:532519. DOI:10.1155/2012/532519
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    • "At sites of blood vessel injury, platelets are activated to induce blood coagulation and form aggregates at the site of the damaged endothelium to prevent hemorrhage and thereby protects us from fatal bleedings. Besides their role in hemostasis, platelets have been shown to contribute to nonhemostatic processes such as wound healing, immunity, angiogenesis, cardiovascular disease and tumor metastasis (Felding-Habermann et al., 1996; Jurk and Kehrel, 2005). A connection between platelets and malignant disease has been recognized since the end of the 19th century, when Armand Trousseau observed increased thrombotic events in patients that were later diagnosed with cancer (Trousseau, 1865). "
    Tumor Angiogenesis, 02/2012; , ISBN: 978-953-51-0009-6
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