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von Willebrand Factor (VWF) Is not required for red blood cell retention in clots in mice (View publication)


Modifiers of fibrin(ogen) and association with disease. Clot formation, structure, and stability are influenced by conditions present during fibrin generation. Abnormal clot formation is observed in several diseases.

Modifiers of fibrin(ogen) and association with disease (View publication)


FXIIIa cross-linking during fibrin formation. Fibrinogen is a hexamer composed of 2 Aα- (purple), 2 Bβ- (blue), and 2 γ-chains (green). During coagulation, thrombin cleaves N-terminal fibrinopeptides from the Aα- and Bβ-chains, producing fibrin monomers which polymerize into protofibrils and subsequently, fibers. FXIIIa increases clot stability by introducing ε-N-(γ-glutamyl)-lysyl cross-links between residues in the γ- and α-chains of fibrin monomers within individual fibers. FXIIIa first introduces cross-links between γ-chains (forming γ-γ dimers) and subsequently between γ- and α-chains (forming high-molecular-weight species [γ-multimers, α-polymers, and αγ-hybrids]).

FXIIIa cross-linking during fibrin formation (View publication)


Venous thrombi contain regions of high red blood cell (RBC) and fibrin content. Left) Gross image of a segment of human venous thrombus (pulmonary embolus) collected at autopsy at UNC Hospitals. Note the presence of darker (RBC rich) regions. Image courtesy of Vincent J. Moylan, Jr, MS, PA(ASCP), UNC at Chapel Hill, School of Medicine. Right) Transmission electron micrograph of a pulmonary embolus showing the ‘brick-and-mortar’ organization of RBCs and fibrin within the thrombus.

Venous thrombi contain regions of high RBC and fibrin content (View publication)


Interplay between abnormalities in blood components, the vasculature, and blood flow contribute to the development of arterial thrombosis. Arterial thrombosis involves the formation of platelet-rich “white clots” that form after rupture of atherosclerotic plaques and exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothelial breach, in a high shear environment. TM = thrombomodulin; II = prothrombin; IIa = thrombin; Fgn = fibrinogen; TF = tissue factor.
Arterial thrombosis. Abbreviations: TM, thrombomodulin; II, prothrombin; IIa, thrombin; Fgn, fibrinogen; TF, tissue factor (View publication)


Tissue factor-initiated coagulation

Schematic of cell-mediated procoagulant activities leading to fibrin clot formation


Distribution of fibrin fibers above a cell surface using Laser Scanning Confocal Microscopy and Transmission Electron Microscopy
Distribution of fibrin fibers above a cell surface (Laser Scanning Confocal Microscopy and Transmission Electron Microscopy)

Normal and Hemophilic Clots

Confocal micrographs of normal vs. hemophilic clots (View publication)


Networks formed under flow and stasis

Scanning electron micrographs of networks formed under flow (left) and stasis (right) (View publication)


Fibrinogen synthesis and expression (View publication)


Contributions of FXIIIa to clot stability (View publication)


FXIIIa mediates RBC retention in thrombi (View publication)


Venous thrombosis. Abbreviations: TM, thrombomodulin; EPCR, endothelial protein C receptor; II, prothrombin; IIa, thrombin; TF, tissue factor; Fgn, fibrinogen; RBC, red blood cells (View publication)


Scanning electron micrograph of a whole blood clot

Transmission electron micrographs of a whole blood clot

Contributions from cells, plasma, and blood flow (Virchow's Triad) regulate fibrin formation and therefore, fibrin network structure and stability

Virchow’s Triad (View publication)


Elevated Fibrinogen and Thrombosis

Effects of elevated fibrinogen on thrombus development in carotid artery (left) and saphenous vein (right)
(View publication)