Clotting is a critical function of blood--without the ability to clot, any small injury would quickly lead to catastrophic loss of blood volume, and death. Instead, under normal conditions, injured blood vessels have the ability to send cellular distress signals that initiate the largely protein-mediated clotting process, rapidly producing a domino effect that culminates in formation of a blood clot and cessation of bleeding.
Initiation of Signal
One of the first roles of protein in the clotting process is that proteins in the blood vessel walls, if exposed, send cellular distress signals. von Willebrand factor, one of the best studied of these proteins, is normally sequestered between the outer and inner lining of blood vessels, and isn't exposed to blood. Dr. Lauralee Sherwood in her textbook, Human Physiology, explains that if a blood vessel becomes cut or otherwise damaged, the von Willebrand factor protein comes in contact with blood. This causes the factor to send a distress signal that initiates further steps in the coagulation cascade.
Factor Involvement
The next steps in clotting are complex, and involve many different proteins called clotting factors. The factors activate one another, explains Dr. Sherwood, producing a so-called "cascade" effect that, once initiated, quickly leads to activation of all involved factors. The ultimate goal of the factor cascade is activation of the final factor, called factor X. Clotting proceeds quickly because factors don't need to be produced or secreted by cells; they're constantly present in blood, albeit in an inactive form. Inactive proteins, called zymogens, offer advantages over active proteins in situations such as clotting. If active clotting factors were present in the blood all the time, blood would clot without cause. If clotting factor proteins had to be produced as needed, clotting would take a long time. Instead, each factor activates the protein beneath it in the factor cascade, working only on factor proteins close to the injury, and only for so long as bleeding continues.
Final Pathway
In their book Biochemistry, Drs. Mary Campbell and Shawn Farrell explain the final steps in clotting. Factor X cleaves off a piece of the zymogen prothrombin, converting it into the active protein thrombin. Thrombin cleaves off a piece of the zymogen fibrinogen, converting it into the active protein fibrin. Fibrin is a sticky, spiderweb-like protein that forms a "net" in the area of a broken blood vessel. The sticky net catches red blood cells, platelets, and other materials from the blood to form a dam-like blood clot, which stops bleeding.
References
- "Human Physiology"; Lauralee Sherwood, Ph.D.; 2004
- "Biochemistry"; Mary Campbell, Ph.D. and Shawn Farrell, Ph.D.; 2005
