Platelet Adhesion and Aggregation
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- Опубликовано: 26 авг 2024
- Developed and produced for www.MechanismsI... by Mechanisms in Medicine Inc.
Animation description: Platelet adhesion and aggregation.
In flowing blood, red cells predominate in the axial stream, while the biconvex disc-shaped platelets are marginated along the vessel wall where they are well-positioned to monitor the integrity of the endothelium. The normal endothelium provides a non-adhesive surface to circulating platelets.
However, when vessel wall injury occurs, for example, by cutting or severing of a vessel, or as shown here, by a puncture, and there is endothelial damage, the initial response of platelets is that of adhesion to collagen fibres in the exposed subendothelium.
Collagen is one of the most thrombogenic components of the subendothelial matrix responsible for the initiation of platelet adhesion. A number of adhesive receptors on the platelet surface membrane interact either directly or indirectly with collagen.
Initial binding of platelets is considered to occur via the integrin α2β1 (GPIa-IIa) receptor, which allows for further binding to collagen via the GPVI receptor, initiating transmembrane and, subsequently, intracellular signalling. Adhesion of platelets to the exposed subendothelium is influenced by shear rates. At high shear, α2β1 and GPVI are not sufficient to initiate binding to collagen, and binding of the GPIb-IX-V receptor to von Willebrand factor -- abbreviated here as V.W.F. -- that is immobilized on collagen, becomes essential in platelet adhesion.
Platelet adhesion at the site of vessel wall damage initiates activation events that result in aggregation. Adherent platelets undergo a dramatic shape change to an irregular sphere with multiple filipodia spreading on the subendothelium increasing their area of surface contact.
Adherent platelets also secrete or release the contents of their storage granules - the alpha and dense granules -- by an exocytic process. This provides a high local concentration of effector molecules essential for platelet plug formation at the site of vascular injury. For example, the aggregating agent A.D.P. is released from the dense granules.
Platelet activation stimulates the formation of another aggregating agent, thromboxane A2 -- abbreviated here as T.X.A2 -- via the arachidonic acid cascade -- details are shown in Figure 26-5.
A.D.P., thromboxane A2 and thrombin bind to specific platelet membrane receptors -- details are shown in Table 26-1 -- and stimulate aggregation on and around the platelets adherent to the subendothelium via receptor-mediated signal transduction events. Aggregation is an active metabolic process: binding of any of the agonists to their respective membrane receptors initiates signalling pathways that ultimately convert integrin αIIbβ3 -- or GPIIb-IIIa - from a low affinity resting state to a high-affinity activated state for binding extracellular soluble ligands such as plasma fibrinogen and von Willebrand factor -- fibrinogen is shown here.
The transmission of an intracellular signal leads to disruption of the complex between the cytoplasmic tails of αIIbβ3, followed by a conformational change in its extracellular globular head domains from a bent to an extended state, promoting the binding to fibrinogen and von Willebrand factor.
Divalent fibrinogen and multivalent von Willebrand factor function as bridges between αIIbβ3 receptors on adjacent activated platelets, thus allowing platelet aggregation to proceed.
In this way, the large and complex metabolic repertoire of platelets allows them to effectively perform their primary physiological role, that of supporting hemostasis upon tissue trauma to form a platelet plug that arrests blood loss from a vascular injury.
To learn more, go to www.MechanismsI... -- a freely available, educational resource that combines the clinical expertise of hematologists, oncologists, and related researchers with instructive visuals and animations. Essential concepts pertaining to the science and biology of clinical hematology are presented.
very complex but excellent, thank you for the detailed description
rainbow
@unclehelicopter
At this time there is no publicly available video on just that topic. Thanks for the comment though.
Thank you for this video!
is GP IIb/IIIa receptor activated by ADP, TxA2, or Thrombin binding to their respective receptors on the platelet cell membrane?
I left my textbook to better understand this...I like the video but damn..thats a lot of info to remember...
Excellent and very nice thank you so much sir
Great video for summing up the important concept of platelet activation and aggregation!
Thanks a lot for the video. Too many non high-yield terms though... But overall, super informative.
superb video thank you
Wow!! Such a reliable informations.
Thank you- excellent!!
i like when the aIIbB3 receptors spring up like a little worm
so does vasoconstriction occur first followed by platelet activation???????
Awesome thanks for upload
Awesome video!
GREAT HELP. The video is easier to understand.
awesome, very detailed.
Question, what cleaves fibrinogen into fibrin? What does the fibrin do?
So fibrinogen connects platelets via alpha 2b beta 3, does fibrin interact with platelets or are they just making fibrin mesh/gel/matrix?
Helpful video
Great video! Is there another one also for the formation of the fibrin plug?
nice video. now if only i could remember everything I just watched lol
Thanks you very much. It is very useful for me.
Thank you very much sir ❤❤❤.
great video
I love to see it
Thank you so much
Isn't fibrinogen converted to fibrin before?
+Kat H
No, fibrinogen is converted to fibrin during coagulation. In this video, it's platelet aggregation. Coagulation comes after.
Excellent!!!
good work
fantastic!
thank you very much that helped alot
Thank you!!
Nice 👍
Any heart surgeon or researcher?
Thank you so much ✌
very helpful
Great
Good
thrombin cleaves fibrinogen thus transforming it into fibrin
WINNING.
@unclehelicopter
For essential concepts pertaining to the science and biology of clinical hematology you may check one of our projects - MechanismsinHematology.ca, specifically, the "Coagulation Cascade" chapter.
Thank you.
Fantastic:)
helpful vid
thx guy
Thank u :) u helped a lot!
which book is this video affiliated with?
"Mechanisms in Hematology", Paperback 3rd Edition (2002);
by Lyonel G. Israels; Esther D. Israels (Author).
A newer version, 4th Edition (2014), is available for download as an iPad App www.mechanismsinhematology.com/site/app.aspx
Anyone here from cells at work?
anone anone!
All hail anone!
hataraku saibou my ninja
Glycoprotein 1b
helpfull, thank you
where is figur 26 5
Thank you for your interest. It can be found in chapter 26 at www.mechanismsinhematology.com. Registration is free, and you will have access to the entire "Mechanisms in Hematology" online resource.
非常好！！！
WHAT ABOUT FIBRIN??
i hate med school so much
umut, so why enter?
Don’t pursue a path that ends in a career you’re not interested in.
You will be miserable for life.
Nice video, but it doesn't explain the mechanism of Thromboxane A2...
so many uncooked chickens
Thank you very much sir ❤❤❤.