Have no fear..Fibrin is here!

Have no fear! Fibrin is here! Have a clotting issue? No problem! Fibrin here will get you fixed and on your way in no time! You may be asking yourself; what is fibrin, and what does it do? Why, it is the most spectacular protein of them all! It helps in the clotting or coagulation of blood to aid in healing. It is made from fibrinogen and is converted into fibrin when thrombin interacts with it. Even research backs how awesome this protein is! It was found that hPDC has enhanced binding when cultured on fibrin substrates. The result of this experiment shows that when combined with hPDC, fibrin sealants could debilitate osteogenesis. 

Yet more research shows that fibrinogen and fibrin stimulate vascular smooth muscle cells (SMC's) to adhere to each other and interact. This shows that the adhesion and migration of SMC's can be directly linked to fibrin and fibrinogen. It also shows that fibrin is involved in many vascular diseases.

To add onto the glory of fibrin; fibrinogen is synthesized in the liver and then converted to thrombin into an insoluble fibrin network. This network, along with platelets enable haemostasis when the endothelium is broken. Concentration of fibrin effects thrombin synthesis as well as fibrinolysis--which takes place in the vessel lumen. It has been shown that fibrinolysis is part of what helps tissues to remodel. 

What more reason does one need to be convinced that Fibrin really is, pardon my colloquialism, the bomb diggity?

[1] J. Demol, J. Eyckmans, S.J. Roberts, F.P. Luyten, and H. Van Oosterwyck. Does Tranexamic Acid Stabilized Fibrin Support the Osteogenic Differentiation of Human Periostium Derived Cells?. European Cells and Materials Vol. 21 2011 (pages 272-285) [Internet]. http://www.ecmjournal.org/journal/papers/vol021/pdf/v021a21.pdf

[2] Naito, M. Effects of fibrinogen, fibrin and their degradation products on the behavior of vascular smooth muscle cells. Japanese Journal of Geriatrics Vol.37 , No.6(2000)pp.458-463. [Internet]. http://www.journalarchive.jst.go.jp/english/jnlabstract_en.php?cdjournal=geriatrics1964&cdvol=37&noissue=6&startpage=458

[3] Juhan-Vague, I., Hans, M. From fibrinogen to fibrin and its dissolution. Laboratoire d'Hématologie, CHU Timone, INSERM EPI 9936-13385 Marseille. [Internet] http://www.ncbi.nlm.nih.gov/pubmed/14556455 

Fibrin Article Summaries

[1]J. Demol in “Does Tranexamic Acid Stabilized Fibrin Support the Osteogenic Differentiation of Human Periostium Derived Cells?" examined the in vitro differentiation, the viability, and the proliferation of hPDC's when grown on a fibrin sealant with osteogenic conditions. This allowed them to evaluate the "impact of dimensionality of hPDC-fibrin constructs" (pg 283) when examining what influences fibrin has on hPDC. It was found that when cultured on fibrin substrates vs. a plastic culture, hPDC  was "enhanced" on the fibrin. Proliferation rates and expression of osteogenic markers were found to be reduced when in a 3D culture. This would indicate that fibrin sealants would, if applied along with hPDC's, debilitate osteogenesis.

[2]Naito, M. in "Effects of fibrinogen, fibrin and their degradation products on the behavior of vascular smooth muscle cells," looks at how fibrin and fibrinogen effect the behavior and migration of vascular smooth muscle cells (SMCs). Fibrinogen and FIbrin stimulate SMCs to adhere to each other and to migrate. The findings in this experiment show that adhesion and migration of SMCs is caused by fibrin. ThIs is without the presence of chemotactic and chemokinetic substances. This indicates that fibrin is important in the development of vascular diseases like atherosclerosis and thrombosis. 

[3]Juhan-Vague, I., and Hans, M. in "From fibrinogen to fibrin and its dissolution" examine what fibrinogen and fibrin are and what they do. Fibrinogen is synthesized in the liver and converted by thrombin to an "insoluble fibrin network" that along with platelets, enable haemostasis when endothelium is broken. It is also shown that fibrin regulates thrombin and "factor XIII activities" and fibrinolysis. Fibrinolysis takes place in the vessel lumen, and is found to be inhibited by plasminogen activator inhibitor-1 (PA-1). It has also been shown the fibrinolysis is part of what helps tissues remodel. It is possible that an excess of PA-1 could help cause the development  of atherothrombosis. Another recent study done with mice shows that an excess of PA-1 can cause an inhibition to gain weight. 

[1] J. Demol, J. Eyckmans, S.J. Roberts, F.P. Luyten, and H. Van Oosterwyck. Does Tranexamic Acid Stabilized Fibrin Support the Osteogenic Differentiation of Human Periostium Derived Cells?. European Cells and Materials Vol. 21 2011 (pages 272-285) [Internet]. http://www.ecmjournal.org/journal/papers/vol021/pdf/v021a21.pdf

[2] Naito, M. Effects of fibrinogen, fibrin and their degradation products on the behavior of vascular smooth muscle cells. Japanese Journal of Geriatrics Vol.37 , No.6(2000)pp.458-463. [Internet]. http://www.journalarchive.jst.go.jp/english/jnlabstract_en.php?cdjournal=geriatrics1964&cdvol=37&noissue=6&startpage=458

[3] Juhan-Vague, I., Hans, M. From fibrinogen to fibrin and its dissolution. Laboratoire d'Hématologie, CHU Timone, INSERM EPI 9936-13385 Marseille. [Internet] http://www.ncbi.nlm.nih.gov/pubmed/14556455

Fibrin: First Look