Platelets are tiny, anucleated blood components that circulate throughout the bloodstream. Their primary function is to stop bleeding when a blood vessel is injured. They form a plug at the site of damage, which helps create a blood clot. This process, known as hemostasis, prevents excessive blood loss.
Basic Platelet Appearance
Platelets are the smallest blood cells, measuring 2 to 3 micrometers in diameter when inactive. They have a discoid, or lens-like, shape in their resting state. Platelets do not contain a nucleus.
These fragments originate in the bone marrow from large cells called megakaryocytes. Megakaryocytes extend protrusions into blood vessels, which are sheared off by flowing blood to form platelets. Platelets circulate for 7 to 10 days before being cleared from the body.
Essential Internal Components
The platelet’s interior contains several structures that contribute to its function. Granules are the most abundant internal components, categorized into alpha and dense granules. Alpha granules (50 to 80 per platelet) are the largest and contain proteins involved in hemostasis, such as growth factors, fibrinogen, and von Willebrand factor.
Dense granules (2 to 7 per platelet) are smaller and store non-protein substances like adenosine diphosphate (ADP), serotonin, and high levels of calcium. Mitochondria, responsible for energy production, are also present (10 to 11 per platelet). Lysosomes, holding hydrolytic enzymes, are also found within the platelet.
The cytoskeleton, composed of actin and microtubules, provides structural support and enables shape changes during activation. Microtubules help maintain the discoid shape of resting platelets. The open canalicular system (OCS) is a network of channels connecting the platelet’s surface to its interior, facilitating molecule secretion and absorption.
A separate internal membrane system, the dense tubular system (DTS), stores calcium ions and is involved in prostaglandin synthesis, including thromboxane A2. Unlike the OCS, the DTS does not connect directly to the plasma membrane. Both the OCS and DTS regulate calcium levels and signaling pathways within the platelet.
The Platelet Surface
The outermost layer of the platelet is its plasma membrane, important for interacting with its environment. Embedded within this membrane are glycoproteins that act as receptors. These receptors allow platelets to bind to other cells and components of the blood vessel wall.
Two receptor complexes on the platelet surface are Glycoprotein Ib-IX-V (GP Ib-IX-V) and Glycoprotein IIb/IIIa (GP IIb/IIIa). GP Ib-IX-V mediates the initial attachment of platelets to damaged blood vessels by binding to von Willebrand factor. GP IIb/IIIa is the most abundant platelet receptor, with 60,000 to 80,000 copies per platelet, and is primarily involved in platelet aggregation by binding to fibrinogen.
The platelet surface is also covered by a coat called the glycocalyx. This carbohydrate-rich layer provides protection and plays a role in interactions with other cells and molecules. The integrity of these surface proteins and the glycocalyx is important for proper platelet function.
How Structure Enables Function
The structures within and on the platelet work together to enable its hemostatic functions. Surface receptors, such as GP Ib-IX-V, allow platelets to initially adhere to the site of vascular injury by recognizing exposed proteins like von Willebrand factor. This initial adhesion triggers platelet activation.
During activation, the cytoskeleton, composed of actin and microtubules, facilitates a change in platelet shape from a disc to a spiny sphere. This shape change increases the platelet’s surface area and promotes interactions with other platelets. Activated platelets then express the GP IIb/IIIa receptor, allowing them to bind fibrinogen and aggregate with other platelets to form a plug.
Internal granules also contribute to function. Upon activation, alpha and dense granules release their contents through the open canalicular system into the surrounding environment. This secretion of factors like ADP, serotonin, and growth factors recruits more platelets to the injury site and strengthens the developing clot. The dense tubular system’s calcium stores are released, playing a part in signaling pathways that enhance platelet activation and aggregation.