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Phospholipids, tissue factor and the platelet plug

Posted Nov 16 2009 10:02pm
Q. I have a question about forming the platelet plug. It saysin the 6th slide on the first page that phospholipids are exposed. Phospholipids where and how does platelet aggregation affect that? If this is in the subendothelium why weren’t they exposed upon ripping or whatever caused the endothelial damage? The next slide moves to tissue factor is exposed. Is the tissue factor the phospholipids in the subendothelium?
A. The phospholipids referred to on the 6th slide are part of the platelet cell membrane. The platelet membrane contains many different kinds of phospholipids on its surface. This is important because many of the coagulation factors (for example, the factor Xa-Va complex) require a phospholipid surface to exert their effects. During platelet aggregation, some of the phospholipids undergo important changes, making them more available to the coagulation factors.
So to restate slide 6, here is how a platelet plug is formed:
1. The endothelium gets ripped up, which exposes subendothelial proteins (like collagen) to the
blood.
2. The platelets see these subendothelial proteins, and they stick to them using von Willebrand
factor (this step is called platelet adhesion).
3. As the platelets adhese, they flatten out and release their granules (which have a lot of
functions, one of which is to attract other platelets).
4. Other platelets come to the adhesion site, and they stick down onto the platelets that are
already there (this step is called aggregation).
5. Now the platelet plug is formed. One cool thing about the platelet plug – in addition to its function
of plugging the hole in the vessel – is that the platelet membrane provides a phospholipid
surface which is essential for many of the coagulation factors. In fact, when platelets
aggregate, certain phospholipids in their membranes become even more available to be used
by the coagulation factors.
Tissue factor is a separate thing. It is the substance that initiates the whole coagulation cascade in vivo (so that’s why it’s listed as the first step in the “Fibrin seals up the plug” slide). It’s present in different areas of the body (in the subendothelium, in some inflammatory cells, and perhaps even in little locked-up microparticles in the blood). It is not present in active form in the blood until it’s needed for coagulation. So when the endothelium is ripped up (or when inflammatory cells decide to release it, or when the little microparticles get a signal to open up), tissue factor is exposed to the blood, and it binds to factor VIIa, and the cascade proceeds along the extrinsic pathway.

plug

Q. I have a question about forming the platelet plug. Where are the phospholipids that get exposed, and how does platelet aggregation affect that? If this is in the subendothelium why weren’t they exposed upon ripping or whatever caused the endothelial damage? Also, what is tissue factor?

A. The phospholipids you’re referring to are part of the platelet cell membrane. The platelet membrane contains many different kinds of phospholipids on its surface. This is important because many of the coagulation factors (for example, the factor Xa-Va complex) require a phospholipid surface to exert their effects. During platelet aggregation, some of the phospholipids undergo important changes, making them more available to the coagulation factors.

Here is how a platelet plug is formed:

1. The endothelium gets ripped up, which exposes subendothelial proteins (like collagen) to the blood.

2. The platelets see these subendothelial proteins, and they stick to them using von Willebrand factor (this step is called platelet adhesion).

3. As the platelets adhese, they flatten out and release their granules (which have a lot of functions, one of which is to attract other platelets).

4. Other platelets come to the adhesion site, and they stick down onto the platelets that are already there (this step is called aggregation).

5. Now the platelet plug is formed. One cool thing about the platelet plug – in addition to its function of plugging the hole in the vessel – is that the platelet membrane provides a phospholipid surface which is essential for many of the coagulation factors. In fact, when platelets aggregate, certain phospholipids in their membranes become even more available to be used by the coagulation factors.

Tissue factor is a separate thing. It is the substance that initiates the whole coagulation cascade in vivo. It’s present in different areas of the body (in the subendothelium, in some inflammatory cells, and perhaps even in little locked-up microparticles in the blood). It is not present in active form in the blood until it’s needed for coagulation. So when the endothelium is ripped up (or when inflammatory cells decide to release it, or when the little microparticles get a signal to open up), tissue factor is exposed to the blood, and it binds to factor VIIa, and the cascade proceeds along the extrinsic pathway.

A different kind of plug: the image of Claes Oldenberg’s giant three-way plug at the Tate was taken by jovike ( http://www.flickr.com/photos/49503078599@N01/54082836/ ), under cc license.

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