1. First, platelets adhere to damaged blood vessels and then to each other forming a plug that can stop minor bleeding. This process is mediated by von Willebrandt factor, a large (104 kD) multimeric plasma glycoprotein of subunit mass 225 kD. This protein binds to both a specific receptor on the platelet membrane and to the collagen and possibly other components of the subendothelial membrane.
2. As the platelets aggregate, they release several physiologically active substances, including serotonin (5-hydroxytryptamine) and thromboxane A2, which stimulates vasoconstriction, thereby reducing the blood flow at the injury.
1. Partly by inhibitory compounds secreted by endothelial cells , such as nitric oxide
andprost ac yc li n\ue000 [aprostagl andin (any of various oxygenated unsaturated
cyclic fatty acids of animals that perform a variety of hormonelike actions (as in
controlling blood pressure or smooth muscle contraction)that is a metabolite of
arachidonic acid, inhibits platelet aggregation, and dilates blood vessels].
Disruption of the endothelium by trauma, or by a disease such as atherosclerosis, allows
platelets to come in contact with and adhere to sub-endothelial matrix. Adhesion is the
first stage of platelet function. Platelets tend to stick to the exposed ends of injured blood
vessels. Actually, they adhere to any rough surface, particularly to the collagen (the chief
Collagen is not only an important substrate for platelet adhesion but also a binding site
for vWf in the sub-endothelium ( Savage et al 1998). A number of platelet proteins
interact with collagen besides\u03b12 \u03921. Other that interact include\u03b1IIb \u03923, GPIV, GPVI and
two other proteins with a molecular weight of 65,00 and 85,000 molecular weight protein
(Clemetson et. Al 1999). Clinical reports suggest that\u03b12 \u03921 and BPVI are the
physiological platelet receptors for collagen (Moroi et al. 1989, Mieuwenhuis et al. 1985,
and Arai et al. 1995)).
When platelets contact collagen, their shapes change drastically, and numerous spiny
processes begin to protrude from their membranes. At the same time, they tend to stick to
each other with fibrinogen forming a platelet plug in the vascular break. This starts the
second phase of platelet function aggregation. In contrast to adhesion, platelet
aggregation is an active metabolic process in which platelet agonist binding to specific
membrane receptor initiates signaling pathways that enable the integrins\u03b1IIb\u03923 to bind
soluble macromolecular ligands, such as fibrinogen or vWf (Bennett 1996). The
fibrinogen or vWf bound to a\u03b1IIb\u03923 cross-links platelets into a hemostatic plug or
Platelets are important for blood clotting and provide a good example of how cell-cell
interactions are modulated by controlling integrin activity. The\u03b1IIb \u03923 integrin normally is
present on the plasma membrane of platelets but is unable to bind the blood protein
fibrinogen or the other protein ligands. Only after binding collagen or thrombin in a
forming clot activates the platelet can\u03b1IIb \u03923 integrin bind fibrinogen. This interaction
accelerates the formation of the clot. Platelet activation is accompanied by a
conformational change in the\u03b1IIb \u03923 integrin. The nature of this change is unknown, but
as platelet activation also involves a major change in the platelet cytoskeleton. This
change probably involves binding of a cytoskeletal protein to the integrin cytosolic
domain. Patients with genetic defects in the\u03b23 integrin subunit are prone to excessive
Unstimulated platelets do not aggregate in circulation since they do not bind fibrinogen.
Antagonists such as ADP, epinephrine, thrombin, or prostaglandin endoperoxides
stimulate platelets exposing fibrinogen receptors to associate with\u03b1IIb \u03923 integrin, which
results in fibrinogen binding and subsequent platelet aggregation.
Platelets are the smallest corpuscular components of human blood (diameter 2-4\u00b5m) - the
physiological number varies from 150,000 to 300,000/mm3 blood. Despite their
appearance on the face of it platelets are not cells, as they are not provided with a
nucleus. The origin of platelets is the bone marrow. Megakaryocytes as the results of
mitotic proliferation of a committed progenitor cells liberate platelets as the end product
of protrusions of their membrane and cytoplasm. The typical shape of resting platelets is
discoid (Figure 2 & 3), upon activation they undergo a shape change to a globular form
with pseudopodia (up to 5\u00b5m long).
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